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World J Gastroenterol. Jun 7, 2023; 29(21): 3241-3256
Published online Jun 7, 2023. doi: 10.3748/wjg.v29.i21.3241
Emerging role of the gut microbiome in post-infectious irritable bowel syndrome: A literature review
Vasile Valeriu Lupu, Cristina Mihaela Ghiciuc, Gabriela Stefanescu, Laura Bozomitu, Iuliana Magdalena Starcea, Anca Adam Raileanu, Ancuta Lupu, Faculty of General Medicine, “Grigore T. Popa” University of Medicine and Pharmacy, Iasi 700115, Romania
Cristina Maria Mihai, Faculty of General Medicine, Ovidius University, Constanta 900470, Romania
Alina Popp, Faculty of General Medicine, “Carol Davila” University of Medicine and Pharmacy, Bucharest 020021, Romania
Maria Oana Sasaran, Faculty of General Medicine, “George Emil Palade” University of Medicine, Pharmacy, Science and Technology, Targu Mures 540142, Romania
ORCID number: Vasile Valeriu Lupu (0000-0003-2640-8795); Cristina Mihaela Ghiciuc (0000-0003-1791-0425); Gabriela Stefanescu (0000-0002-1394-8648); Cristina Maria Mihai (0000-0001-8844-0593); Alina Popp (0000-0002-7809-5762); Maria Oana Sasaran (0000-0001-8156-7460); Iuliana Magdalena Starcea (0000-0002-3937-7425); Anca Adam Raileanu (0000-0003-1979-8174); Ancuta Lupu (0000-0001-8147-3632).
Author contributions: Lupu VV, Bozomitu L, Starcea IM, Adam Raileanu A, and Lupu A wrote the initial draft; Ghiciuc CM, Stefanescu G, Mihai CM, Popp A, and Sasaran MO reviewed and edited the article; Ghiciuc CM, Stefanescu G, Mihai CM, Popp A, Sasaran MO, Bozomitu L, Starcea IM, Adam Raileanu A and Lupu A contributed equally with Lupu VV to this article.
Conflict-of-interest statement: Authors declare no conflict of interests for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
Corresponding author: Anca Adam Raileanu, MD, PhD, Attending Doctor, Faculty of General Medicine, “Grigore T. Popa” University of Medicine and Pharmacy, 16 University Street, Iasi 700115, Romania.
Received: February 16, 2023
Peer-review started: February 16, 2023
First decision: April 2, 2023
Revised: April 4, 2023
Accepted: May 8, 2023
Article in press: May 8, 2023
Published online: June 7, 2023
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Post-infectious irritable bowel syndrome (PI-IBS) is a particular type of IBS, with symptom onset after an acute episode of infectious gastroenteritis. Despite infectious disease resolution and clearance of the inciting pathogen agent, 10% of patients will develop PI-IBS. In susceptible individuals, the exposure to pathogenic organisms leads to a marked shift in the gut microbiota with prolonged changes in host-microbiota interactions. These changes can affect the gut-brain axis and the visceral sensitivity, disrupting the intestinal barrier, altering neuromuscular function, triggering persistent low inflammation, and sustaining the onset of IBS symptoms. There is no specific treatment strategy for PI-IBS. Different drug classes can be used to treat PI-IBS similar to patients with IBS in general, guided by their clinical symptoms. This review summarizes the current evidence for microbial dysbiosis in PI-IBS and analyzes the available data regarding the role of the microbiome in mediating the central and peripheral dysfunctions that lead to IBS symptoms. It also discusses the current state of evidence on therapies targeting the microbiome in the management of PI-IBS. The results of microbial modulation strategies used in relieving IBS symptomatology are encouraging. Several studies on PI-IBS animal models reported promising results. However, published data that describe the efficacy and safety of microbial targeted therapy in PI-IBS patients are scarce. Future research is required.

Key Words: Gut microbiome, Infectious gastroenteritis, Irritable bowel syndrome, Post infection syndrome, Pathophysiology, Inflammation

Core Tip: Acute infectious gastroenteritis can trigger the onset of irritable bowel syndrome (IBS), leading to the development of post-infectious IBS (PI-IBS). PI-IBS is a clinical entity associated with gut dysbiosis. Alterations in the gut microbiome can affect the gut-brain axis, visceral sensitivity, intestinal barrier, intestinal secretion, gut motility, and immune activation, which in turn can cause IBS symptoms. A better understanding of PI-IBS is necessary to develop more targeted and effective treatments. Therapies targeting the microbiome, such as probiotics, antibiotics, diet, and fecal microbiota transplants, improve IBS symptoms. There is a lack of evidence of their efficiency in PI-IBS.


Irritable bowel syndrome (IBS) is the most frequently encountered disorder of gut-brain interactions[1], with a worldwide prevalence ranging between 7% and 15% of the general population[2,3]. According to the Rome IV criteria, it is characterized by mild to severe recurrent abdominal pain and bloating associated with alterations in bowel habits in the absence of organic disease or biochemical abnormalities[4]. Due to its symptoms, IBS is thought to be a disabling disease. It generates significant healthcare costs, reduces work productivity and school attendance, and decreases the health-related quality of life of the affected individuals[5,6]. Despite being a frequent entity in current gastroenterology practice, the physiopathology of IBS is not fully understood. It is considered to be a complex multifactorial disorder affected by several factors such as age, sex, genetics, diet, psychosocial status, altered microbiota, subclinical inflammation, and hypersensitivity of the neural network[7,8]. In recent years, accumulating evidence has suggested that the alteration of the gut microbiota plays an important role in the pathophysiology of IBS, as gut microbes exert effects on the host immune system, on gut barrier function, and on the brain-gut axis[9,10].

Acute infectious gastroenteritis [bacterial-Campylobacter species[11], Salmonella species[12,13], Escherichia coli (E. coli)[14], Shigella[15], Clostridium difficile (C. difficile)[16], viral-norovirus[17], rotavirus[18], severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)[19], and protozoal-Giardia[20]] has been shown to be one of the strongest risk factors for the development of post-infectious IBS (PI-IBS), a distinct condition in which IBS diagnostic criteria are met[21,22]. PI-IBS occurs after the resolution of a gastrointestinal-related infection and the clearance of the inciting pathogen, in a patient without a prior history of IBS symptoms[22,23]. IBS clinical features usually develop 6-18 mo after the infectious gastroenteritis episode[24]. PI-IBS management strategies involve nonpharmacologic and pharmacologic therapies. Current guidance relies on IBS treatment experience, as there is a lack of evidence-based recommendations for PI-IBS treatment[1]. The aim of this review is to analyze the current literature and to describe the role of the human gut microbiota on PI-IBS physiopathology. The main questions to be answered include which long-term consequences of acute enteric infections may serve as triggers to PI-IBS and whether the acute enteric infection associated dysbiosis and its recovery can be used to predict PI-IBS development. Additionally, under discussion is whether there is a specific microbial signature associated with PI-IBS, as most studies of PI-IBS combine patients infected by varying pathogens, thus generating a considerable variability of outcomes. The gut microbiota modulation and its potential therapeutic implications in PI-IBS in terms of efficacy and safety continue to be a subject of debate and highlight the need for specific treatment protocols. A better characterization of the relationship between gut-associated dysbiosis and PI-IBS progression will lead the way to personalized medicine and the individualized management of each patient.


A globally accepted definition of PI-IBS is not currently available in the literature. Most authors consider PI-IBS as a form of IBS for which the symptoms, as specified in the Rome IV criteria, appear after the resolution of an acute gastroenteritis episode in patients without any IBS symptomatology before the gastrointestinal infection[1,4]. In 2019, the Rome Foundation Working Group proposed symptomatic diagnostic criteria for PI-IBS based on the Rome IV criteria (Figure 1), as there are no sensitive and specific diagnostic markers available yet[25]. Considering the predominant bowel pattern graded on the Bristol stool scale, PI-IBS can be classified as diarrhea-predominant IBS (IBS-D), constipation-predominant (IBS-C), mixed bowel habits (IBS-M), and unclassified[1,26]. A bowel pattern is considered predominant when it is ≥ 25% of the time as either hard/lumpy (IBS-C), loose/watery (IBS-D), or both (IBS-M)[1]. PI-IBS patients are more likely than sporadic IBS patients to present a diarrhea-predominant phenotype. The association between each patient and a PI-IBS subtype is important for disease management and therapy[22].

Figure 1
Figure 1 Diagnostic criteria for post-infection irritable bowel syndrome (based on Rome IV criteria). 1Mentioning the exact date of onset of irritable bowel syndrome (IBS) symptomatology can also be suggestive for post-infectious IBS; 2Irregular bowel movements can be experienced even before the onset of the acute gastroenteritis episode (but not in association with frequent pain, as an IBS characteristic). IBS: Irritable bowel syndrome; PI-IBS: Post-infectious irritable bowel syndrome.

While most pathogen agents cause self-limiting acute gastroenteritis, subsequent chronic alteration may persist in some genetically predisposed individuals[27]. According to several studies, about 1 in 10 individuals with an acute episode of gastroenteritis will develop PI-IBS[21,28]. A 2017 meta-analysis reported that the incidence of PI-IBS more than a year after the acute episode of gastroenteritis was 14.5%[29]. Epidemiologic data of the reported incidence and prevalence vary across the literature, in part due to the methodological heterogeneity, including the criteria used to define IBS (Rome criteria I, II, III, or IV)[3,16,22]. Moreover, there is evidence that the data might be underestimated due to the high incidence of infectious gastroenteritis and the poor recall of milder episodes, as the diagnosis relies on self-reported symptom clusters[2,21,30].

Female sex, a young age, certain psychological factors before or during acute infectious gastroenteritis (anxiety, depression, somatization, and/or neuroticism), and genetic predisposition (carriers of the TLR9, CDH1, and IL6 genes) seem to increase the risk of developing PI-IBS[29,31]. The severity of the acute infectious episode also seems to increase the probability of developing PI-IBS after the gastroenteritis resolution[29]. The risk of PI-IBS is doubled when diarrhea lasts > 7 d and is tripled when diarrhea lasts > 21 d. Other symptoms such as abdominal cramps, weight loss, and bloody stools are also associated with an elevated risk, with abdominal cramps increasing the PI-IBS risk four times. Fever is not mentioned as a risk factor[32]. Moreover, it might have a protective action, representing the host’s response to the infectious injury[33]. The risk of IP-IBS remains high for at least 2 to 3 years post infection[22].

Various pathogens have been reported as related to PI-IBS development. A systematic review evaluating the prevalence and risk factors of PI-IBS after acute gastroenteritis by specific pathogens revealed the fact that the evidence indicated a similar risk for bacterial pathogens, while for viral and parasitic gastroenteritis, the data were limited[34]. However, a recent study found the incidence of PI-IBS to be higher in patients with Campylobacter jejuni (C. jejuni) gastroenteritis, compared to other etiologic agents such as bacteria, viruses, or protozoa[35]. When comparing different pathogens, protozoal enteritis shows the highest risk for PI-IBS development, followed by bacterial and then viral[33,36]. Bacterial infections seem to generate more PI-IBS cases than viral gastroenteritis probably due to the fact that the mucosal damage and inflammation caused by bacteria is often greater than that caused by viral agents[37].

There is a strong association between travelers’ diarrhea and PI-IBS. Self-reports of exposure seem to result in a higher PI-IBS occurrence than laboratory-confirmed cases of travelers’ diarrhea, but further studies are needed to confirm this finding[38]. Culture-confirmed infections, either bacterial or viral, seem to present an equally increased risk of PI-IBS as nonspecific gastrointestinal infections[39]. However, viral gastroenteritis is more likely to develop transient forms of PI-IBS than bacterial episodes[40]. The significant decrease in the PI-IBS prevalence from 19% to 4% one year after a viral infection may be due to the less invasive nature of the pathogen, perhaps avoiding a stronger host response[29]. During the recent pandemic, the novel coronavirus SARS-CoV-2 displayed its potential to generate gastrointestinal manifestations[41,42]. It seems that the prevalence of gastrointestinal symptoms in coronavirus disease 2019 (COVID-19) patients is around 10%, and it is following an increasing trend[43,44]. A multicenter study from 2020 reported that digestive symptoms such as diarrhea, vomiting, and abdominal pain were present in 50.5% of COVID-19 patients, while other studies concluded that the incidence of diarrhea in the same category of patients varied from 2% to 20%[41,45,46]. A recent study found an incidence of 11.6% of IBS, according to the Rome IV criteria, with symptom onset following COVID-19 infection[41]. Another group of researchers reported similar results, with 10% of the included patients with an acute episode of SARS-CoV-2 in their medical history meeting the Rome IV criteria for IBS 6 mo after the viral infection. Three percent of them had gastrointestinal symptoms during COVID-19[47]. Noviello et al[48] found an incidence of PI-IBS in 26.2% of patients. The risk of developing de novo IBS post-COVID-19 increases in patients with gastrointestinal symptoms present during the active viral infection. Similar to noninfectious IBS, the risk is higher in female patients. The presence of severe disease markers, such as an oxygen requirement and high procalcitonin levels, increases the risk of post-COVID-19 IBS[49]. Another similar study reported that patients with dyspnea at time of admission and a history of allergies and chronic treatment with proton pump inhibitors had an increased risk of developing post-COVID-19 IBS[50].

Compared to sporadic IBS, PI forms of the disease might have a better outcome[2]. The prognosis of PI-IBS appears favorable with the spontaneous and gradual resolution of symptoms in most patients[22]. However, one longitudinal follow-up study showed that 15% of patients with post-infection IBS remained symptomatic 8 years after disease onset[28].


Available studies have failed to give a clear holistic picture on the underlying pathophysiology of PI-IBS. As IBS is a multifactorial disease, it has been hypothesized that the development of PI-IBS could result from the interplay of fecal microbiota, the immune response of the host, and the psychological factors[51], as illustrated in Figure 2. The current conceptual framework regarding the pathophysiologic mechanism for PI-BS suggests that the exposure to pathogenic organisms leads to the alteration of the gut microbiome. PI-IBS is associated with hyperplasia of enterochromaffin (EC) cells and increased counts of neutrophils, mast cells, and T cells in the colonic mucosa. It is believed that gastrointestinal infections stimulate the immune system causing low-grade inflammation leading to PI-IBS[52].

Figure 2
Figure 2 Conceptual model for post-infectious irritable bowel syndrome. PI-IBS: Post-infectious irritable bowel syndrome.

It was reported that patients with PI-IBS often present an increased visceral pain perception known as visceral hypersensitivity (VHS). The incomplete resolution of the immune response to acute infectious injury might facilitate the persistence of a microscopic inflammation of the bowel, activating and sensitizing pain-sensing nerves[53]. A persistent low-grade inflammation of the bowel is thought to trigger PI-IBS symptoms, by aberrant activation of intrinsic and extrinsic nerves. The increased numbers of immune cells and the enhanced cytokine signaling play an important role in the underlying mechanism of PI-IBS pathophysiology[54]. A group of researchers found an increased IL-1β mRNA expression in rectal tissue biopsies after an acute episode of infectious gastroenteritis. Patients with a Campylobacter enteritis were found to present increased EC cell numbers, intraepithelial lymphocytes, and intestinal permeability up to one year after the infectious episode[55], while patients with PI-IBS following a Shigella gastroenteritis had an increased number of mast cell in the terminal ileum[56]. These cells release mediators such as histamine, IL-1β, IL-6, and TNF-α, mediators that can stimulate or sensitize visceral nociceptors and possibly generate the abdominal pain in PI-IBS[54]. Excessive secretion of IL-8 is a hallmark of Campylobacter pathogenesis, being initiated by the host recognition of the pathogen-associated lipooligosaccharide[57,58]. Another study on PI-IBS patients, however, found no evidence of increased inflammatory gene expression or infiltrating inflammatory cells in biopsies and no increase in cytokine levels[54]. Similarly, no difference was reported in the number of T lymphocytes or proinflammatory cytokines between PI-IBS patients and infected healthy volunteers, 3 years after a Salmonella infection[59]. Another study on a large cohort found similar results, with no difference in serum cytokines and mucosal cytokine expression between PI-IBS patients and healthy volunteers[60]. γδT cells are a subset of T cells involved in initiating inflammatory responses and can acquire the capacity of inducing various cytokines. A recent study of Dong et al[61] found that the Vδ1 γδ T cells subset from PI-IBS patients remarkably proliferated, activated, and produced abundant IL-17. In these patients, the IFN-γ level remained unchanged, as proof of the fact that the local IL-17 could participate in the intestinal pathological disorder during PI-IBS, as the major proinflammatory cytokine[61]. Furthermore, a rodent study concluded that the upregulation of A2AR increased PI-IBS by promoting the T17 polarization of CD4+ T cells[62]. In their study, Balemans et al[54] reported that although initiated by inflammation, the pronociceptive changes seen in PI-IBS patients were mediated by the Hrh1 receptor sensitization of TRPV1 signaling, suggesting that similar to the “standard” IBS12, Hrh1 antagonism may represent an interesting new target for treatment of PI-IBS[54]. In conclusion, the presence of low-grade inflammation is an inconsistent finding in PI-IBS, as it might be an interim event following gastroenteritis that is superseded by another more persistent change in the gut microenvironment[54].

Increased intestinal permeability was shown to be an early event in PI-IBS physiopathology, associated with low-grade inflammation[1]. Patients with PI-IBS and high fecal proteolytic activity presented in vivo and ex vivo distal gut permeability that depended on the fecal level of proteolytic activity[63]. Following a mixed infection of enterohemorrhagic E. coli (EHEC) O157:H7 and C. jejuni during a waterborne outbreak of bacterial gastroenteritis, there was reported an increased intestinal permeability[58]. EHEC is known for its deleterious impact on the epithelial barrier[64]. Giardia duodenalis (G. duodenalis), a protozoan pathogen also implicated in promoting PI-IBS development, is well known to disturb the homeostatic barrier function through several mechanisms[65].

Viral gastroenteritis is a known risk factor for the PI onset of IBS. There are many studies describing the relation between norovirus infection and PI-IBS. As a conclusion to their study, Porter et al[66] suggested that dysmotility disorders may follow viral infections. A high incidence of functional gastrointestinal disorders was reported in patients who suffered from a norovirus gastroenteritis[66]. Similarly, another two studies reported an increased prevalence of PI-IBS in patients who experienced an acute episode of gastroenteritis during a confirmed norovirus outbreak[40,67]. It is thought that norovirus infection can cause epithelial barrier dysfunction, increased intestinal permeability, a reduction in the villous surface area and villous height, and a mucosal immune response with an increase in cytotoxic intraepithelial T cells, impairing the gut’s sensory-motor function[67].

COVID-19, an immunologic and inflammatory response associated with low-grade inflammation and mucosal injury, caused the development of IBS features in genetically predisposed individuals. Patients with PI-IBS can present high levels of macrophages and T lymphocytes in intestinal samples, increased levels of calproctin and fecal cytokines, such as IL-8; all these were found in COVID-19 patients, as well as the presence of virus-specific IgA, together with increased blood levels of proinflammatory cytokines[68,69]. Similar to IBS, the altered intestinal permeability associated with gut dysbiosis and with an alteration of the neuromuscular function might also be involved in PI-IBS onset[67].

On the other hand, the pandemic led to a stressful situation, anxiety, and depression. These factors resulted in other diseases related to psychological stress and the nervous system similar to IBS[70,71]. Farsi et al[41] in their study found that psychological stress had no significant influence on COVID-19-induced IBS symptoms[41]. However, another similar study reported that COVID-19 had adverse effects on both GI and psychological symptoms among individuals with functional dyspepsia-IBS overlap syndrome[70]. Similarly, another study concluded that the COVID-19 pandemic increased psychosocial stress and gastrointestinal symptoms in patients already known to have IBS[72]. The interaction between the gut-brain axis disturbances and genetic and psychosocial factors can contribute to IBS development[41]. Psychological stress acts as a trigger in developing IBS through its adverse effects on intestinal permeability and motility and hypersensitivity to visceral pain. Acute and chronic stressful situations lead to cortico-tropin-releasing hormone secretion, activating the hypothalamic-pituitary-adrenal axis and creating new premises for IBS onset. Stress-induced dysbiosis can modulate the neuro-immune-endocrine systems and interfere with the brain-gut axis[73,74].


Due to the bioavailability of nutrients, the human gastrointestinal tract harbors the largest concentration and diversity of microbiota of the human body. Healthy adult gastrointestinal microbiota are represented by five primary bacteria phyla: Firmicutes (synonym Bacillota) and Bacteroides (synonym Bacteroidota) phylum predominate the microbiota, while Actinobacteria (synonym Actinomycetota), Proteobacteria (synonym Pseudomonadota), and Verrucomicrobia phylum are found in modest proportions[75]. The gut microbiota have a dynamic composition, influenced by many intrinsic and extrinsic factors, such as genetic inheritance, birth mode, breastfeeding duration, age, sex, diet, and drugs[75-77]. The alteration of the healthy microbial structure leads to dysbiosis, resulting in various gastrointestinal disorders, systemic metabolic diseases, and neurological impairments[75].

During an acute infectious gastroenteritis, there is a decline in the gut’s microbial diversity[78]. There are several mechanisms explaining the disruption of the indigenous microbiota. One would be directly throughout pathogen agent-microbiota interaction. Secondly, the alteration of the microbiota might occur via the host’s mucosal immune response, or there is the possibility of a combination of the two presented mechanisms[27,79]. In rodents, Salmonella enterica serovar typhimurium was shown to induce the loss of 95% of the total bacterial numbers of the intestinal tract, 7 d after the infectious episode[80]. G. duodenalis and C. jejuni can directly alter the composition of human gut microbiota[81]. Aside from the predominance of the etiologic bacterial pathogen, certain native taxa of the gut microbiome such as Streptococci, Fusobacteria, and Campylobacter, can also increase their numbers throughout the acute episode but also in the weeks following the bacterial infection[82,83].

Immediately after acute gastroenteritis with Vibrio cholerae (V. cholerae), increased levels of V. cholerae, Streptococcus, Fusobacterium, and Campylobacter species were found during a 16S rRNA gene polymerase chain reaction (PCR) analysis of the infected patients’ stool samples. Two months after the first assessment, there was a decrease in V. cholerae, Streptococcus, Fusobacterium, and Campylobacter species, while Ruminococcus obeum, Collinsella aerofasciens, Ruminococcus torques, Eubacterium rectale, and Faecalibacterium prausnitzii increased their levels as a marker of recovery from the infection[82].

As for gastroenteritis triggered by viral agents, the alterations in the microbiota seem to be less consistent. The immune response to the viral injury is usually less harmful, resulting in a decreased diversity and the expansion of Proteobacteria species in some patients with viral gastroenteritis[83]. A study including patients with all-cause traveler’s diarrhea investigated their gut microbial composition using fecal samples. In diarrheal patients, there was a decreased Bacteroidota/Bacillota ratio and changes in β-diversity, compared to healthy travelers who displayed an unexpected increased abundance of Bacillota phylum (Streptococcus and Lactococcus genera). Stool samples of patients with confirmed norovirus infection had an increased diversity of species characterizing their microbiota during the active infection, including Clostridium XIVb, Bilophilia, Alistipes, Barnesiella, and Roseburia species[84]. When assessing the gut microbiome correlation in symptomatic and asymptomatic patients infected with norovirus, Patin et al[85] found no significant difference between the alpha and beta diversity of the two groups studied. The symptomatic subjects presented relatively more species of Bacillota phylum, especially in the order Clostridia, while Bacteroidota phylum displayed fewer species than the asymptomatic subjects, particularly in the Bacteroidia order. In asymptomatic patients, three members of the genus Parasutterella and one in the Nitrosomonadaceae family were found in higher levels. The increased levels of Bacteroidota in the asymptomatic individuals suggest that its presence could improve the host’s effort of resisting enteric viral infection or neutralizing its pathogenicity and symptoms[85]. Another study on Chinese patients with diarrhea of viral etiology reported a decreased diversity in the gut microbiota at stool sample examination, when compared to healthy individuals. Bacillota phylum with species of Enterococcus, Peptostreptococcaceae, Incertae Sedi, Shigella, Weissella, and Clostridium dominated the microbiota during the acute episode, while beneficial bacteria such as Bacteroides vulgatus, Bifidobacterium, and Lactobacillus species were found in decreased amounts[83]. Nelson et al[86] also tried to characterize the stool microbiota in norovirus-infected human patients. Their research found similarities between infected patients’ and uninfected healthy individuals’ microbiota. However, in a small number of infected patients there was found a significantly altered microbiome characterized by a reduced relative number of Bacteriodota and a corresponding increase in Pseudomonadota. Interestingly, the increased level of Pseudomondota phylum was due to a single operational taxonomic unit of E. coli[86]. This finding raises the concern that the alteration in gut microbiota during an acute viral gastroenteritis exposes the affected patients to some possible long term gastrointestinal complications.

SARS-CoV-2 infected patients seem to present an altered gut microbiota, characterized by the depletion of anti-inflammatory butyrate-producing bacteria and the enrichment of taxa with proinflammatory properties[87,88]. The Alpha and beta diversity index values appear to be significantly lower than in healthy individuals, all through the active infection and the recovery period[87,89]. Furthermore, an important reduction in the major bacterial phylum composition and diversity was also observed[90]. Ruminococcusm gnavus and Bacteroides vulgatus were found in increase amounts in post-acute COVID-19 patients’ microbiomes, while Faecalibacterium prausnitzii, known for its anti-inflammatory proprieties, was characterized as decreased, when compared to healthy individuals[70].

Streptococcus, Enterococcus, and Corynebacterium species, well known as opportunistic pathogens, seem to be found in higher amounts in COVID-19 patients’ stools than in healthy individuals[87]. Fusicatenibacter, Romboutsia, Intestinibacter, Actinomyces, and Erysipelatoclostridium species could actually be used as biomarkers in order to identify COVID-19 positive patients[91]. There is proof that the development of PI-IBS may be predicted by the composition of the salivary microbiome during acute SARS-CoV-2 infection[40,92]. Butyrate-producing bacteria showed an inverse correlation with IBS symptom onset 6 mo post-acute viral infection[93]. The gut microbiota composition was reported to be correlated with proinflammatory cytokine levels, as proof of its contribution to the immune response. The Faecalibacterium genus, belonging to the Clostridia class, was found to be decreased in COVID-19 patients during the acute episode and was inversely correlated with the IL-8 and IL-12 serum levels. The same study reported an enrichment of the Actinomycetota phylum and the Propionibacteriaceae family, which was positively correlated with the gp130/sIL-6Rb level[90]. The Streptococcus species was also associated with an increased expression of proinflammatory cytokines such as IL-18, TNF-α, and IFN-γ[87]. In contrast, IFN-gamma and IL-28A/IFN-12 levels were found to be negatively correlated to the class Clostridia, reduced in abundance in COVID-19 patients[90]. Changes in the microbiome composition were also identified in COVID-19 patients without antibiotic exposure. Depletion of beneficial commensal species and enrichment of opportunistic pathogenic bacteria, such as Clostridium hathewayi, Actinomyces viscosus, and Bacteroides nordii, were found in COVID-19 patients’ stool samples. According to Zuo et al[94], the disease severity and the baseline abundance of certain genera and strains might be in close relationship, as the gut microbiota might actively influence the immune system response. Moreover, it appears that 50% of COVID-19 patients had an active intestinal infection, even in cases with no gastrointestinal complaints[94]. The deleterious effect of SARS-CoV-2 infection on beneficial gut microbiota seems to persist even after disease resolution, sustaining the possibility of the gut microbiome alteration’s role in PI-IBS pathogenesis[95]. The intestinal infection persisted despite respiratory viral clearance[19,94]. There were cases described, where dysbiosis was persistent 30 d after the acute viral episode, suggesting the long-term influence of COVID-19 on gut microbiota[96]. Opportunistic pathogens such as Collinsella aerofaciens, Collinsella tanakaei, Streptococcus infantis, and Morganella morganii have been found in large amounts in stool samples with high SARS-CoV-2 infectivity. In stool samples with low-to-no viral infectivity, there were higher amounts of Parabacteroides merdae, Bacteroides stercoris, and Lachnospiraceae bacterium 1_1_57FAA, some of these within important role in augmenting host immunity[19,94]. Current evidence suggests that a high microbial exposure to Gram-negative bacteria could offer protective effects against COVID-19, possibly due to the increased interferon type I levels[43]. These findings sustain the idea that the gut homeostasis may suffer some alterations during the acute COVID-19 episode, independent from the presence of gastrointestinal symptoms, alterations that can persist beyond disease resolution[73]. There is evidence that COVID-19-induced impairment of the gut-lung axis might create predisposing factors for IBS development[43,97].

Moreover, there is evidence that microbiota composition prior to infection may also influence the possibility of developing an acute infection as well as PI-IBS[33]. Dicksved et al[98] reported that an increased abundance of Bacteroidota in pre-employment stool samples of abattoir workers increased the risk of developing a C. jejuni infection during the period of employment[98]. A Clostridiales-predominant microbiota type has a protective role, as an individual with such intestinal microbiota is more likely to return to a state of eubiosis after the remission of the infectious episode and pathogen clearance. A Bacteroidota predominant community, in contrast, may increase the risk of long-term dysbiosis after the acute episode’s resolution[21].

Although the gut microbiota profile of IBS patients has been evaluated in several studies, there is not the same consistency of data regarding PI-IBS patients’ gut microbiome alteration. In their study of the real-time PCR assay of rectal epithelium RNA expression, Jalanka-Tuovinen et al[51] concluded that the intestinal microbiota of PI-IBS patients were significantly different from healthy individuals but similar to patients with IBS-like symptoms (PI bowel disease, PI-IBS and IBS-D). They identified an “index of microbial dysbiosis” (IMD) that characterized the intestinal microbiota of PI-IBS. The IMD included 27 genus-like microbial groups including a twelvefold increased level of Bacteroidota phylum, including as Bacteroides and Prevotella species. The Bacillota phylum was less abundant, with decreased levels of various uncultured Clostridiales and Clostridium clusters. Moreover, dysbiosis was associated with gastrointestinal symptoms’ severity and not with psychological symptoms. Dysbiosis was also associated with biopsy findings, such as increased levels of eotaxins, mast cells, and goblet cells and decreased EC cells[51]. Similar results were obtained by Sundin et al[99], when analyzing the mucosal and fecal microbiota of patients with PI-IBS. The fecal microbiota composition of PI-IBS patients was significantly different from the fecal microbiota of IBS patients and healthy individuals. Patients with PI-IBS had a reduced mucosal and fecal microbial diversity, with reduced levels of Bacillota, including Clostridium clusters IV and XIVa, and increased Bacteroidota, including Bacteroides species. The reduced diversity of the fecal microbiota was associated with increased activated lymphocytes in the lamina propria. At the level of major butyrate producer bacteria abundance, there was no difference identified between the PI-IBS patients and healthy individuals. Unlike Jalanka-Tuovinen et al[51], the reduced diversity of the microbiota was associated with the presence of psychological symptoms[99]. In PI-IBS patients, the Bacteroidota phylum seems to have a relatively greater abundance of microbes than in healthy individuals, while Bacillota phylum display a relative reduction in representative members in the gut microbiota[78]. The main findings are summarized in Table 1.

Table 1 Alterations of the gut microbiota observed during acute gastroenteritis and during post-infectious irritable bowel syndrome.
Sample and techniques
Microbiota alterations
Other findings
Jalanka-Tuovinen et al[51], 201411 postinfection IBS, 11 postinfection bowel dysfunction, 12 postinfection without bowel dysfunction, 12 IBS-D, 11 healthy controls adults16S rRNA gene phylogenetic microarray analysis with HITChip, 16S rRNA gene qPCR with group and species-specific primers of feacal sampleIndex of microbial dysbiosis” comprised of 27 genus-like groups including: ↑Bacteroidota including various Bacteroides and Prevotella species, ↓Bacillota including various uncultured Clostridiales, and Clostridium clustersDysbiosis was associated with bowel, not psychological symptoms; Dysbiosis associated biopsy findings: ↑eotaxin, mast cells, goblet cells, ↓enterochromaffin cells; Dysbiosis associated RNA expression pathways: ↑serotonin transport, condensed chromosome, B cell antigen receptor, ↓caspase
Hsiao et al[82], 20147 adults with V. cholerae AGE history, 50 healthy children, 12 healthy adults 16S rRNA gene PCR, V4 region analysis of faecal sampleOne week after AGE: ↑V. cholerae Streptococcus spp Fusobacterium spp Campylobacter sppTwo months after AGE (recovery period): ↓V. cholerae Streptococcus spp Fusobacterium spp Campylobacter spp, ↑species indicating recovery Ruminococcus obeum, Collinsella aerofasciens Ruminococcus torques, Eubacterium rectale Faecalibacterium prausnitzii
Ma et al[83], 201113 Adenovirus diarrhea, 13 Rotavirus diarrhea, 13 Astrovirus diarrhea, 13 Norvirus diarrhea, 6 control children16S rRNA gene PCR, V3 region analysis of faecal sample↓Diversity in diarrheal patients, ↑Enterococcus, Peptostreptococcaceae, Incertae Sedi, Shigella, Weissella sppBacteroides vulgatus Bifidobacterium, Lactobacillus spp
Youmans et al[84], 2015111 all-cause traveler’s diarrhea/12 healthy travelers16S rRNA gene PCR, V3 and V5 regions analysis of faecal sample Bacteroidota: Bacillota ratio in diarrheal patients; ↑Species diversity during norovirus infection; ↑Clostridium XIVb Bilophilia Alistipes Barnesiella, Roseburia spp during norovirus infectionBacillota phylum Streptococcus Lactococcus spp in healthy travelers (unexpected)
Patin et al[88], 20204 symptomatic and 5 asymptomatic norovirus infected adults16S rRNA gene analysis of faecal samplePost norovirus challenge: ↑Bacillota phylum, particularly Clostridia, ↓Bacteroidota PseudomonadotaPrior to norovirus challenge: Asymptomatic patients had ↑Bacteroidota phylum and ↓Clostridia compared to symptomatic
Nelson et al[86], 201238 norovirus infection, 22 healthy controls16S rRNA gene 454 pyrosequencing, V3-V5 regions analysis of faecal sampleA subset (approximately 1/5) patients with norovirus had: ↓diversity, ↑Pseudomonadota phylum, Enterobacteriaceae familyEscherichia coli diversity and virulence was not associated with norovirus infection
Cheng et al[87], 2022COVID-19 acute and recovery phase; Non COVID-19Meta-analysis of 16S rRNA microbial data↓Ruminococcus Faecalibacterium Roseburia, Coprococcus genus, ↑Fusobacterium Streptococcus in recovery/post-recovery COVID-19 compared to non COVID-19Clostridium clostridioforme, ↑Bifidobacterium breve in COVID-19 compared to recovery/post-recovery COVID-19
Liu et al[93], 202268 COVID-19 patients, 68 non-COVID-19 patientsShotgun metagenomic sequencingAt 6 mo follow up 76% developed PACS; Non-PACS showed recovered gut microbiome profile at 6 mo comparable to that of non-COVID-19 controls; ↑Ruminococcus gnavus, Bacteroides vulgatus and ↓Faecalibacterium prausnitzii in PACSButyrate-producing bacteria, including Bifidobacterium pseudocatenulatum and Faecalibacterium prausnitzii showed the largest inverse correlation with PACS at 6 mo
Zuo et al[95], 202015 Acute COVID-patients, 6 community acquired pneumonia patients, 15 healthy controlsShotgun metagenomic sequencingAntibiotic naïve patients ↑Clostridium hathewayi, Actinomyces viscosus, and Bacteroides nordii compared with controls; COVID-19 with antibiotic use ↓Faecalibacterium prausnitzii, Lachnospiraceae bacterium 5_1_63FAA, Eubacterium rectale, Ruminococcus obeum, and Dorea formicigenerans compared with COVID-19 naïve patientsBaseline abundance of Coprobacillus, Clostridium ramosum, and Clostridium hathewayi correlated with COVID-19 severity: There was an inverse correlation between abundance of Faecalibacterium prausnitzii and disease severity; Depletion of symbionts and enrichment of opportunistic pathogens persisted after clearance of SARS-CoV-2
Yeoh et al[96], 2021100 COVID-19 patients, 78 non COVID-19 controlsShotgun sequencing total DNA extraction from stool sample Patients with COVID-19 were depleted in Faecalibacterium prausnitzii, Eubacterium rectale and several bifidobacterial species, which remain low up to 30 d from disease resolutionComposition of the gut microbiota in patients with COVID-19 is concordant with disease severity and magnitude of plasma concentrations of several inflammatory cytokines, chemokines and blood markers of tissue damage
Sundin et al[99], 201513 PI-IBS patients, 19 general IBS patients, 16 healthy controlsHITChip for mucosal and fecal microbiota↓Mucosal and faecal diversity Bacillota phylum including Clostridium clusters IV and XIVa, ↑Bacteroidota phyum including Bacteroides sppReduced diversity was associated with psychological symptoms and increased activated lamina propria lymphocytes. Did not find a difference in major butyrate producer abundance

Acute gastroenteritis, as mentioned above, can alter the gut microbiota, initiating the underlying mechanisms of PI-IBS. Modulation of the microbiota can be performed using probiotics, symbiotics, prebiotics, and antibiotics or by performing a fecal microbial transplantation, with the purpose of downregulating inflammation, improving barrier function, and reducing visceral sensitivity[100]. To date, there is no specific practice guideline or treatment strategies for PI-IBS. Different drug classes can be used for treating PI-IBS similar to patients with IBS in general[37].

Probiotics are known to be “live microorganisms that, when administered in adequate amounts, confer a health benefit on the host”[101]. Lactobacillus casei DG (LC-DG) and its postbiotic were shown to attenuate the inflammatory mucosal response in an ex vivo organ culture model of PI-IBS-D[102]. Similarly, Hong et al[103] reported that probiotic administration (Lactobacillus acidophilus LA5, Bifidobacterium animalis subsp. lactis BB12, and Saccharomyces cerevisiae var. boulardii) decreased proinflammatory cytokine levels in both the control and PI-IBS induced mice[103].

Saccharomyces boulardii, given 750 mg/day for a period of 6 wk, was reported to improve the quality of life and the cytokine profile in PI-IBS patients[104]. Bifidobacterium infantis, M-63 1 × 109 cfu/sachet/day given daily for 3 mo, restored the normal composition of the gut microbiota and improved mental health in individuals with post-flood acquired IBS[105].

Given the current evidence that serotonin levels are increased in PI-IBS patients, serotonin-based therapy is a treatment option that deserves further study[106]. Cao et al[107] proved that an Lactobacillus rhamnosus supernatant had a positive effect on serotonin transporter (SERT) expression in colon tissues of rats with PI-IBS. By modulating the microbial composition, the serotonergic imbalance can be restored, followed by the improvement in IBS symptoms[107]. Another similar study on an animal model evaluated the efficacy of a Bacillus subtilis (B. subtilis), Enterococcus faecium, and Enterococcus faecalis (E. faecalis) supernatant, administrated in PI-IBS rats. The researchers reported that the supernatants could upregulate the expression level of SERT in intestinal cells, mentioning the fact that the combined supernatants of B. subtilis and E. faecalis had a superior effect to the administration of a single supernatant[108]. Studies regarding prebiotic and symbiotic use in PI-IBS patients are not available.

Fecal microbiota transplantation (FMT) is used in order to restore microbial dysbiosis by transferring a healthy microbiome to an individual with an alteration of microbial composition[109]. FMT has shown benefits in IBS patients. However, there is a lack of data on FMT use in PI-IBS. A recent randomized clinical trial assessed FMT’s safety as well as its clinical and microbiological efficacy in patients with PI-IBS. The results demonstrated FMT’s effectiveness compared to traditional pharmacotherapy, its safety, and tolerability[110].

However, FMT could be used in reestablishing the microbiota homeostasis following acute gastroenteritis, with the purpose of decreasing the risk of PI-IBS development. It is known that FMT is recommended for recurrent or refractory C. difficile enterocolitis, as a proved effective therapy[111]. There is evidence that FMT treatment can improve gut microbiota alteration in recovered COVID-19 patients, particularly in those who presented severe gastrointestinal symptomatology during the acute phase[112].

Jin et al[113] assessed the action of rifaximin on the VHS, barrier function, gut inflammation, and microbiota in a PI-IBS mouse model. Rifaximin administration improved the VHS, recovered the intestinal barrier function, and inhibited low-grade inflammation in the colon and ileum, without changing the composition and diversity of the gut microbiota[113]. However, Harris et al[114] and Tuteja et al[115] reported no benefit of rifaximin therapy on PI-IBS patients.

The results of mesalazine’s efficacy in treating PI-IBS patients are contradictory. Lam et al[116] reported a significant improvement in symptoms such as abdominal pain, urgency, and stool consistency, when mesalazine was given to a small group of PI-IBS patients[116]. Bafutto et al[117] found that mesalazine administration in PI-IBS patients decreased the stool frequency and improved its form and consistency, after 30 d of treatment[117]. In contrast, another double-blind controlled trial including a small number of patients with diarrhea predominant PI-IBS reported no positive effect on clinical symptoms or quality of life[118]. However, mesalazine use during the acute infectious gastroenteritis may have a protective effect on PI-IBS development, as reported by a study on patients affected by hemorrhagic enterocolitis with Shiga-like toxin-producing E. coli[119]. Dunlop et al[120] found a significant reduction in the T- lymphocyte counts in the rectal tissue of PI-IBS patients treated with prednisone, although there was no positive effect on the EC cell count or symptom improvement[120].

Bile acid malabsorption may occur after an episode of acute gastroenteritis. It is confirmed that cholestyramine administration can alleviate symptoms in PI-IBS patients, especially with diarrhea symptoms[121]. The information regarding the therapeutic options in PI-IBS are summarized in Table 2.

Table 2 Post-infectious irritable bowel syndrome therapeutic options.
Therapeutic intervention
Compare et al[102], 2017Lactobacillus casei DG + postbiotic↓The inflammatory mucosal response in an ex vivo organ culture model of PI-IBS-D
Hong et al[103], 2019Lactobacillus acidophilus LA5, Bifidobacterium animalis subsp. lactis BB12 and Saccharomyces cerevisiae var. boulardii)↓Pro-inflammatory cytokine levels in both the control and PI-IBS induced mice
Abbas et al[104], 2014Saccharomyces boulardiiImproved the quality of life and the cytokine profile in PI-IBS patients
Lee et al[106], 2017Bifidobacterium infantisRestored the normal composition of gut microbiota and improved mental health among individuals with post-flood acquired IBS
Cao et al[107], 2018Lactobacillus rhamnosus supernatant Had a positive effect on SERT expression in colon tissues of rats with PI-IBS, improving IBS symptoms in PI-IBS rats
Chen et al[108], 2022Enterococcus faecium and Enterococcus faecalis supernatant, in PI-IBS ratsThe supernatants of B. subtilis, Enterococcus faecium, and Enterococcus faecalis can upregulate SERT expression in intestinal epithelial cells and the intestinal tissues in the rat model of PI-IBS
Tkach et al[110], 2022RCT, low FODMAP diet + Otilonium Bromide + a multi-strain probiotic vs FMT procedureFMT proved effectiveness in restoring normal gut microbiota and ameliorating PI-IBS symptoms, compared to traditional pharmacotherapy, as well as a high degree of safety and good tolerability
Liu et al[111], 2021FMT procedureFMT can partially restore the gut dysbiosis in COVID-19 patients by increasing the relative abundance of Actinobacteria (15.0%) and reducing Proteobacteria (2.8%) at the phylum level. At the genera level, Bifidobacterium and Faecalibacterium had significantly increased after FMT
Jin et al[113], 2017Rifamixin in PI-IBS ratsRifaximin alleviated visceral hypersensitivity, recoverd intestinal barrier function and inhibited low-grade inflammation in colon and ileum of PI-IBS rats. Exerts anti-inflammatory effects with only a minimal action on the overall composition and diversity of the gut microbiota
Harris et al[114], 2019Rifamixin vs placebo in veterans with IBSRifaximin was not associated with signifcant improvement in global symptoms, abdominal pain, stool frequency, urgency, bloating, or stool consistency
Tuteja et al[115], 2019Rifamixin vs placebo in veterans with IBSRifaximin was not effective in improving IBS symptoms and QOL in GW veterans with non-constipated IBS
Lam et al[116], 2016Mesalazine vs placeboMesalazine was no better than placebo in relieving symptoms of abdominal discomfort or disturbed bowel habit. Mesalazine did not reduce mast cell percentage area stained. A subgroup of patients with postinfectious IBS may benefit from mesalazine
Bafutto et al[117], 2011Mesalazine in PI-IBS patients compared to non-infective IBS patientsMesalazine reduced key symptoms of postinfectious irritable bowel syndrome and noninfective irritable bowel syndrome with diarrhea patients, with no statistical difference between IBS and PI-IBS
Tuteja et al[118], 2012Mesalazine vs placeboThere was no significant improvement in global symptoms or overall QOL with mesalazine in patients with PI-IBS
Andresen et al[119], 2016Mesalazine during the AGE with STECMesalazine administration during AGE with STEC might be a protective factor for PI-IBS
Dunlop et al[120], 2003Prednisolone vs placeboPrednisolone does not appear to reduce the number of enterochromaffin cells or cause an improvement in symptoms in PI-IBS

Acute gastroenteritis can significantly increase the risk of developing IBS, a chronic gastrointestinal pathology with high health-care utilization. Current studies in humans as well as animal models describe specific host-pathogen interactions that may lead to the onset of post-infection IBS symptoms. There is no curative treatment option for PI-IBS, and patients rely only on symptomatic therapy. There are numerous studies on IBS treatment options. However, there is a lack of data regarding PI-IBS therapeutic management, and there is a great need for evidence-based recommendations in post-acute gastroenteritis IBS.

These advancements in understanding will be helpful in elaborating specific biomarkers used to identify patients with a high risk of developing IBS symptoms following an acute infectious gastroenteritis, as well as designing targeted pharmacotherapy. Microbial restoration, augmentation of barrier function, and targeting VHS remain the most promising areas for therapeutic interventions and represent a future research perspective.


Provenance and peer review: Invited article; Externally peer reviewed.

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Specialty type: Gastroenterology and hepatology

Country/Territory of origin: Romania

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P-Reviewer: Belkova N, Russia; Zamani M, Iran S-Editor: Zhang H L-Editor: A P-Editor: Ma YJ

1.  Drossman DA, Hasler WL. Rome IV-Functional GI Disorders: Disorders of Gut-Brain Interaction. Gastroenterology. 2016;150:1257-1261.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 731]  [Cited by in F6Publishing: 824]  [Article Influence: 103.0]  [Reference Citation Analysis (0)]
2.  Ford AC, Sperber AD, Corsetti M, Camilleri M. Irritable bowel syndrome. Lancet. 2020;396:1675-1688.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 219]  [Cited by in F6Publishing: 333]  [Article Influence: 83.3]  [Reference Citation Analysis (1)]
3.  Oka P, Parr H, Barberio B, Black CJ, Savarino EV, Ford AC. Global prevalence of irritable bowel syndrome according to Rome III or IV criteria: a systematic review and meta-analysis. Lancet Gastroenterol Hepatol. 2020;5:908-917.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 155]  [Cited by in F6Publishing: 327]  [Article Influence: 81.8]  [Reference Citation Analysis (0)]
4.  Mearin F, Lacy BE, Chang L, Chey WD, Lembo AJ, Simren M, Spiller R. Bowel Disorders. Gastroenterology. 2016;.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1781]  [Cited by in F6Publishing: 1617]  [Article Influence: 202.1]  [Reference Citation Analysis (2)]
5.  Canavan C, West J, Card T. The epidemiology of irritable bowel syndrome. Clin Epidemiol. 2014;6:71-80.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 139]  [Cited by in F6Publishing: 374]  [Article Influence: 37.4]  [Reference Citation Analysis (0)]
6.  Spiegel BM. The burden of IBS: looking at metrics. Curr Gastroenterol Rep. 2009;11:265-269.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 110]  [Cited by in F6Publishing: 125]  [Article Influence: 8.3]  [Reference Citation Analysis (0)]
7.  Chen YQ, Yang X, Xu W, Yan Y, Chen XM, Huang ZQ. Knockdown of lncRNA TTTY15 alleviates myocardial ischemia-reperfusion injury through the miR-374a-5p/FOXO1 axis. IUBMB Life. 2021;73:273-285.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 8]  [Cited by in F6Publishing: 12]  [Article Influence: 3.0]  [Reference Citation Analysis (0)]
8.  Ansari MH, Ebrahimi M, Fattahi MR, Gardner MG, Safarpour AR, Faghihi MA, Lankarani KB. Viral metagenomic analysis of fecal samples reveals an enteric virome signature in irritable bowel syndrome. BMC Microbiol. 2020;20:123.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 20]  [Cited by in F6Publishing: 11]  [Article Influence: 2.8]  [Reference Citation Analysis (0)]
9.  Pimentel M, Lembo A. Microbiome and Its Role in Irritable Bowel Syndrome. Dig Dis Sci. 2020;65:829-839.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 65]  [Cited by in F6Publishing: 88]  [Article Influence: 22.0]  [Reference Citation Analysis (0)]
10.  Singh P, Lembo A. Emerging Role of the Gut Microbiome in Irritable Bowel Syndrome. Gastroenterol Clin North Am. 2021;50:523-545.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 6]  [Cited by in F6Publishing: 17]  [Article Influence: 5.7]  [Reference Citation Analysis (0)]
11.  Takakura W, Kudaravalli P, Chatterjee C, Pimentel M, Riddle MS. Campylobacter infection and the link with Irritable Bowel Syndrome: on the pathway towards a causal association. Pathog Dis. 2022;80.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Cited by in F6Publishing: 1]  [Article Influence: 0.5]  [Reference Citation Analysis (0)]
12.  Cambrea SC, Petcu LC, Mihai CM, Hangan TL, Iliescu DM. Influence of environmental factors about evolution of shigellosis in constanta county of Romania. J Environ Prot Ecol. 2019;20:986-994.  [PubMed]  [DOI]  [Cited in This Article: ]
13.  Halichidis S, Balasa AL, Ionescu EV, Iliescu MG, Cambrea SC, Petcu LC, Mihai CM. Evolution of salmonellosis in Constanta area in correlation with environmental factors. J Environ Prot Ecol. 2019;20: 1496-1504.  [PubMed]  [DOI]  [Cited in This Article: ]
14.  Lashermes A, Boudieu L, Barbier J, Sion B, Gelot A, Barnich N, Ardid D, Carvalho FA. Adherent-Invasive E. coli enhances colonic hypersensitivity and P2X receptors expression during post-infectious period. Gut Microbes. 2018;9:26-37.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 16]  [Cited by in F6Publishing: 16]  [Article Influence: 2.3]  [Reference Citation Analysis (0)]
15.  Kim HS, Lim JH, Park H, Lee SI. Increased immunoendocrine cells in intestinal mucosa of postinfectious irritable bowel syndrome patients 3 years after acute Shigella infection--an observation in a small case control study. Yonsei Med J. 2010;51:45-51.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 57]  [Cited by in F6Publishing: 66]  [Article Influence: 4.7]  [Reference Citation Analysis (0)]
16.  Saha S, Sehgal K, Singh S, Grover M, Pardi D, Khanna S. Postinfection Irritable Bowel Syndrome Following Clostridioides difficile Infection: A Systematic-review and Meta-analysis. J Clin Gastroenterol. 2022;56:e84-e93.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Reference Citation Analysis (0)]
17.  Hassan E, Baldridge MT. Norovirus encounters in the gut: multifaceted interactions and disease outcomes. Mucosal Immunol. 2019;12:1259-1267.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 18]  [Cited by in F6Publishing: 17]  [Article Influence: 3.4]  [Reference Citation Analysis (0)]
18.  Baaleman DF, Di Lorenzo C, Benninga MA, Saps M. The Effects of the Rome IV Criteria on Pediatric Gastrointestinal Practice. Curr Gastroenterol Rep. 2020;22:21.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 15]  [Cited by in F6Publishing: 15]  [Article Influence: 3.8]  [Reference Citation Analysis (0)]
19.  Cooney J, Appiahene P, Findlay R, Al-Hillawi L, Rafique K, Laband W, Shandro B, Poullis A. COVID-19 infection causing residual gastrointestinal symptoms - a single UK centre case series. Clin Med (Lond). 2022;22:181-183.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 16]  [Cited by in F6Publishing: 10]  [Article Influence: 5.0]  [Reference Citation Analysis (0)]
20.  Litleskare S, Rortveit G, Eide GE, Hanevik K, Langeland N, Wensaas KA. Prevalence of Irritable Bowel Syndrome and Chronic Fatigue 10 Years After Giardia Infection. Clin Gastroenterol Hepatol. 2018;16:1064-1072.e4.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 40]  [Cited by in F6Publishing: 44]  [Article Influence: 7.3]  [Reference Citation Analysis (0)]
21.  Barbara G, Grover M, Bercik P, Corsetti M, Ghoshal UC, Ohman L, Rajilić-Stojanović M. Rome Foundation Working Team Report on Post-Infection Irritable Bowel Syndrome. Gastroenterology. 2019;156:46-58.e7.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 138]  [Cited by in F6Publishing: 127]  [Article Influence: 25.4]  [Reference Citation Analysis (0)]
22.  Thabane M, Marshall JK. Post-infectious irritable bowel syndrome. World J Gastroenterol. 2009;15:3591-3596.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 101]  [Cited by in F6Publishing: 110]  [Article Influence: 7.3]  [Reference Citation Analysis (4)]
23.  Moshiree B, Heidelbaugh JJ, Sayuk GS. A Narrative Review of Irritable Bowel Syndrome with Diarrhea: A Primer for Primary Care Providers. Adv Ther. 2022;39:4003-4020.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
24.  Ruigómez A, García Rodríguez LA, Panés J. Risk of irritable bowel syndrome after an episode of bacterial gastroenteritis in general practice: influence of comorbidities. Clin Gastroenterol Hepatol. 2007;5:465-469.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 60]  [Cited by in F6Publishing: 63]  [Article Influence: 3.7]  [Reference Citation Analysis (0)]
25.  Ghaffari P, Shoaie S, Nielsen LK. Irritable bowel syndrome and microbiome; Switching from conventional diagnosis and therapies to personalized interventions. J Transl Med. 2022;20:173.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 10]  [Article Influence: 5.0]  [Reference Citation Analysis (0)]
26.  Lewis SJ, Heaton KW. Stool form scale as a useful guide to intestinal transit time. Scand J Gastroenterol. 1997;32:920-924.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1858]  [Cited by in F6Publishing: 1926]  [Article Influence: 71.3]  [Reference Citation Analysis (0)]
27.  Beatty JK, Bhargava A, Buret AG. Post-infectious irritable bowel syndrome: mechanistic insights into chronic disturbances following enteric infection. World J Gastroenterol. 2014;20:3976-3985.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 69]  [Cited by in F6Publishing: 64]  [Article Influence: 6.4]  [Reference Citation Analysis (0)]
28.  Marshall JK, Thabane M, Garg AX, Clark WF, Moayyedi P, Collins SM; Walkerton Health Study Investigators. Eight year prognosis of postinfectious irritable bowel syndrome following waterborne bacterial dysentery. Gut. 2010;59:605-611.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 159]  [Cited by in F6Publishing: 143]  [Article Influence: 10.2]  [Reference Citation Analysis (0)]
29.  Klem F, Wadhwa A, Prokop LJ, Sundt WJ, Farrugia G, Camilleri M, Singh S, Grover M. Prevalence, Risk Factors, and Outcomes of Irritable Bowel Syndrome After Infectious Enteritis: A Systematic Review and Meta-analysis. Gastroenterology. 2017;152:1042-1054.e1.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 233]  [Cited by in F6Publishing: 256]  [Article Influence: 36.6]  [Reference Citation Analysis (1)]
30.  Borgaonkar MR, Ford DC, Marshall JK, Churchill E, Collins SM. The incidence of irritable bowel syndrome among community subjects with previous acute enteric infection. Dig Dis Sci. 2006;51:1026-1032.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 45]  [Cited by in F6Publishing: 40]  [Article Influence: 2.2]  [Reference Citation Analysis (0)]
31.  Villani AC, Lemire M, Thabane M, Belisle A, Geneau G, Garg AX, Clark WF, Moayyedi P, Collins SM, Franchimont D, Marshall JK. Genetic risk factors for post-infectious irritable bowel syndrome following a waterborne outbreak of gastroenteritis. Gastroenterology. 2010;138:1502-1513.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 169]  [Cited by in F6Publishing: 186]  [Article Influence: 13.3]  [Reference Citation Analysis (0)]
32.  Kamp KJ, Cain KC, Utleg A, Burr RL, Raftery D, Luna RA, Shulman RJ, Heitkemper MM. Bile Acids and Microbiome Among Individuals With Irritable Bowel Syndrome and Healthy Volunteers. Biol Res Nurs. 2021;23:65-74.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 20]  [Cited by in F6Publishing: 18]  [Article Influence: 6.0]  [Reference Citation Analysis (0)]
33.  Berumen A, Edwinson AL, Grover M. Post-infection Irritable Bowel Syndrome. Gastroenterol Clin North Am. 2021;50:445-461.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 18]  [Cited by in F6Publishing: 13]  [Article Influence: 4.3]  [Reference Citation Analysis (0)]
34.  Svendsen AT, Bytzer P, Engsbro AL. Systematic review with meta-analyses: does the pathogen matter in post-infectious irritable bowel syndrome? Scand J Gastroenterol. 2019;54:546-562.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 16]  [Cited by in F6Publishing: 21]  [Article Influence: 4.2]  [Reference Citation Analysis (0)]
35.  Iacob T, Țățulescu DF, Lupșe MS, Dumitrașcu DL. Post-infectious irritable bowel syndrome after a laboratory-proven enteritis. Exp Ther Med. 2020;20:3517-3522.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 2]  [Article Influence: 0.5]  [Reference Citation Analysis (0)]
36.  Shariati A, Fallah F, Pormohammad A, Taghipour A, Safari H, Chirani AS, Sabour S, Alizadeh-Sani M, Azimi T. The possible role of bacteria, viruses, and parasites in initiation and exacerbation of irritable bowel syndrome. J Cell Physiol. 2019;234:8550-8569.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 36]  [Cited by in F6Publishing: 39]  [Article Influence: 6.5]  [Reference Citation Analysis (0)]
37.  Sadeghi A, Biglari M, Nasseri Moghaddam S. Post-infectious Irritable Bowel Syndrome: A Narrative Review. Middle East J Dig Dis. 2019;11:69-75.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 9]  [Cited by in F6Publishing: 15]  [Article Influence: 3.0]  [Reference Citation Analysis (0)]
38.  Schwille-Kiuntke J, Mazurak N, Enck P. Systematic review with meta-analysis: post-infectious irritable bowel syndrome after travellers' diarrhoea. Aliment Pharmacol Ther. 2015;41:1029-1037.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 74]  [Cited by in F6Publishing: 66]  [Article Influence: 7.3]  [Reference Citation Analysis (0)]
39.  Donnachie E, Schneider A, Mehring M, Enck P. Incidence of irritable bowel syndrome and chronic fatigue following GI infection: a population-level study using routinely collected claims data. Gut. 2018;67:1078-1086.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 38]  [Cited by in F6Publishing: 43]  [Article Influence: 7.2]  [Reference Citation Analysis (0)]
40.  Marshall JK, Thabane M, Borgaonkar MR, James C. Postinfectious irritable bowel syndrome after a food-borne outbreak of acute gastroenteritis attributed to a viral pathogen. Clin Gastroenterol Hepatol. 2007;5:457-460.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 172]  [Cited by in F6Publishing: 153]  [Article Influence: 9.0]  [Reference Citation Analysis (0)]
41.  Farsi F, Zonooz SR, Ebrahimi Z, Jebraili H, Morvaridi M, Azimi T, Sikaroudi MK, Heshmati J, Khorrami S, Mokhtare M, Faghihi A, Masoodi M. The Incidence of Post-infectious Irritable Bowel Syndrome, Anxiety, and Depression in Iranian Patients with Coronavirus Disease 2019 Pandemic: A Cross-Sectional Study. Turk J Gastroenterol. 2022;33:1033-1042.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 7]  [Reference Citation Analysis (0)]
42.  Hussain I, Cher GLY, Abid MA, Abid MB. Role of Gut Microbiome in COVID-19: An Insight Into Pathogenesis and Therapeutic Potential. Front Immunol. 2021;12:765965.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 44]  [Cited by in F6Publishing: 24]  [Article Influence: 8.0]  [Reference Citation Analysis (0)]
43.  Cheung KS, Hung IFN, Chan PPY, Lung KC, Tso E, Liu R, Ng YY, Chu MY, Chung TWH, Tam AR, Yip CCY, Leung KH, Fung AY, Zhang RR, Lin Y, Cheng HM, Zhang AJX, To KKW, Chan KH, Yuen KY, Leung WK. Gastrointestinal Manifestations of SARS-CoV-2 Infection and Virus Load in Fecal Samples From a Hong Kong Cohort: Systematic Review and Meta-analysis. Gastroenterology. 2020;159:81-95.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1113]  [Cited by in F6Publishing: 1059]  [Article Influence: 264.8]  [Reference Citation Analysis (1)]
44.  Sultan S, Altayar O, Siddique SM, Davitkov P, Feuerstein JD, Lim JK, Falck-Ytter Y, El-Serag HB; AGA Institute. AGA Institute Rapid Review of the Gastrointestinal and Liver Manifestations of COVID-19, Meta-Analysis of International Data, and Recommendations for the Consultative Management of Patients with COVID-19. Gastroenterology. 2020;159:320-334.e27.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 283]  [Cited by in F6Publishing: 276]  [Article Influence: 69.0]  [Reference Citation Analysis (1)]
45.  Pan L, Mu M, Yang P, Sun Y, Wang R, Yan J, Li P, Hu B, Wang J, Hu C, Jin Y, Niu X, Ping R, Du Y, Li T, Xu G, Hu Q, Tu L. Clinical Characteristics of COVID-19 Patients With Digestive Symptoms in Hubei, China: A Descriptive, Cross-Sectional, Multicenter Study. Am J Gastroenterol. 2020;115:766-773.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1160]  [Cited by in F6Publishing: 1147]  [Article Influence: 286.8]  [Reference Citation Analysis (0)]
46.  Montazeri M, Maghbouli N, Jamali R, Sharifi A, Pazoki M, Salimzadeh A, Barzegari B, Rafiei N, Mansouri ES, Hadadi A. Clinical Characteristics of COVID-19 Patients with Gastrointestinal Symptoms. Arch Iran Med. 2021;24:131-138.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 3]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
47.  Austhof E, Bell ML, Riddle MS, Catalfamo C, McFadden C, Cooper K, Scallan Walter E, Jacobs E, Pogreba-Brown K. Persisting gastrointestinal symptoms and post-infectious irritable bowel syndrome following SARS-CoV-2 infection: results from the Arizona CoVHORT. Epidemiol Infect. 2022;150:e136.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Cited by in F6Publishing: 12]  [Article Influence: 6.0]  [Reference Citation Analysis (0)]
48.  Noviello D, Costantino A, Muscatello A, Bandera A, Consonni D, Vecchi M, Basilisco G. Functional gastrointestinal and somatoform symptoms five months after SARS-CoV-2 infection: A controlled cohort study. Neurogastroenterol Motil. 2022;34:e14187.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 11]  [Cited by in F6Publishing: 30]  [Article Influence: 15.0]  [Reference Citation Analysis (0)]
49.  Siyal M, Abbas Z, Ashraf J, Ali Qadeer M, Altaf A. Incidence and predisposing factors for de novo post-COVID-19 irritable bowel syndrome. Eur J Gastroenterol Hepatol. 2023;35:59-63.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 6]  [Reference Citation Analysis (0)]
50.  Marasco G, Cremon C, Barbaro MR, Cacciari G, Falangone F, Kagramanova A, Bordin D, Drug V, Miftode E, Fusaroli P, Mohamed SY, Ricci C, Bellini M, Rahman MM, Melcarne L, Santos J, Lobo B, Bor S, Yapali S, Akyol D, Sapmaz FP, Urun YY, Eskazan T, Celebi A, Kacmaz H, Ebik B, Binicier HC, Bugdayci MS, Yağcı MB, Pullukcu H, Kaya BY, Tureyen A, Hatemi İ, Koc ES, Sirin G, Calıskan AR, Bengi G, Alıs EE, Lukic S, Trajkovska M, Hod K, Dumitrascu D, Pietrangelo A, Corradini E, Simren M, Sjölund J, Tornkvist N, Ghoshal UC, Kolokolnikova O, Colecchia A, Serra J, Maconi G, De Giorgio R, Danese S, Portincasa P, Di Sabatino A, Maggio M, Philippou E, Lee YY, Salvi D, Venturi A, Borghi C, Zoli M, Gionchetti P, Viale P, Stanghellini V, Barbara G; GI-COVID19 study group. Post COVID-19 irritable bowel syndrome. Gut. 2022;.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 14]  [Cited by in F6Publishing: 19]  [Article Influence: 9.5]  [Reference Citation Analysis (0)]
51.  Jalanka-Tuovinen J, Salojärvi J, Salonen A, Immonen O, Garsed K, Kelly FM, Zaitoun A, Palva A, Spiller RC, de Vos WM. Faecal microbiota composition and host-microbe cross-talk following gastroenteritis and in postinfectious irritable bowel syndrome. Gut. 2014;63:1737-1745.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 226]  [Cited by in F6Publishing: 234]  [Article Influence: 23.4]  [Reference Citation Analysis (0)]
52.  Devanarayana NM, Rajindrajith S. Irritable bowel syndrome in children: Current knowledge, challenges and opportunities. World J Gastroenterol. 2018;24:2211-2235.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 53]  [Cited by in F6Publishing: 49]  [Article Influence: 8.2]  [Reference Citation Analysis (2)]
53.  Brierley SM, Linden DR. Neuroplasticity and dysfunction after gastrointestinal inflammation. Nat Rev Gastroenterol Hepatol. 2014;11:611-627.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 179]  [Cited by in F6Publishing: 200]  [Article Influence: 20.0]  [Reference Citation Analysis (0)]
54.  Balemans D, Mondelaers SU, Cibert-Goton V, Stakenborg N, Aguilera-Lizarraga J, Dooley J, Liston A, Bulmer DC, Vanden Berghe P, Boeckxstaens GE, Wouters MM. Evidence for long-term sensitization of the bowel in patients with post-infectious-IBS. Sci Rep. 2017;7:13606.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 32]  [Cited by in F6Publishing: 32]  [Article Influence: 4.6]  [Reference Citation Analysis (0)]
55.  Spiller RC, Jenkins D, Thornley JP, Hebden JM, Wright T, Skinner M, Neal KR. Increased rectal mucosal enteroendocrine cells, T lymphocytes, and increased gut permeability following acute Campylobacter enteritis and in post-dysenteric irritable bowel syndrome. Gut. 2000;47:804-811.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 805]  [Cited by in F6Publishing: 792]  [Article Influence: 33.0]  [Reference Citation Analysis (0)]
56.  Gwee KA, Collins SM, Read NW, Rajnakova A, Deng Y, Graham JC, McKendrick MW, Moochhala SM. Increased rectal mucosal expression of interleukin 1beta in recently acquired post-infectious irritable bowel syndrome. Gut. 2003;52:523-526.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 291]  [Cited by in F6Publishing: 323]  [Article Influence: 15.4]  [Reference Citation Analysis (0)]
57.  Rodiño-Janeiro BK, Vicario M, Alonso-Cotoner C, Pascua-García R, Santos J. A Review of Microbiota and Irritable Bowel Syndrome: Future in Therapies. Adv Ther. 2018;35:289-310.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 106]  [Cited by in F6Publishing: 126]  [Article Influence: 21.0]  [Reference Citation Analysis (0)]
58.  Flynn AN, Wang A, McKay DM, Buret AG. Apoptosis-inducing factor contributes to epithelial cell apoptosis induced by enteropathogenic Escherichia coli. Can J Physiol Pharmacol. 2011;89:143-148.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 6]  [Cited by in F6Publishing: 8]  [Article Influence: 0.6]  [Reference Citation Analysis (0)]
59.  Mearin F, Perelló A, Balboa A, Perona M, Sans M, Salas A, Angulo S, Lloreta J, Benasayag R, García-Gonzalez MA, Pérez-Oliveras M, Coderch J. Pathogenic mechanisms of postinfectious functional gastrointestinal disorders: results 3 years after gastroenteritis. Scand J Gastroenterol. 2009;44:1173-1185.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 38]  [Cited by in F6Publishing: 38]  [Article Influence: 2.7]  [Reference Citation Analysis (0)]
60.  Bennet SM, Polster A, Törnblom H, Isaksson S, Capronnier S, Tessier A, Le Nevé B, Simrén M, Öhman L. Global Cytokine Profiles and Association With Clinical Characteristics in Patients With Irritable Bowel Syndrome. Am J Gastroenterol. 2016;111:1165-1176.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 64]  [Cited by in F6Publishing: 60]  [Article Influence: 7.5]  [Reference Citation Analysis (0)]
61.  Dong LW, Sun XN, Ma ZC, Fu J, Liu FJ, Huang BL, Liang DC, Sun DM, Lan C. Increased Vδ1γδT cells predominantly contributed to IL-17 production in the development of adult human post-infectious irritable bowel syndrome. BMC Gastroenterol. 2021;21:271.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 3]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
62.  Dong LW, Ma ZC, Fu J, Huang BL, Liu FJ, Sun D, Lan C. Upregulated adenosine 2A receptor accelerates post-infectious irritable bowel syndrome by promoting CD4+ T cells' T helper 17 polarization. World J Gastroenterol. 2022;28:2955-2967.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 3]  [Cited by in F6Publishing: 2]  [Article Influence: 1.0]  [Reference Citation Analysis (2)]
63.  Edogawa S, Edwinson AL, Peters SA, Chikkamenahalli LL, Sundt W, Graves S, Gurunathan SV, Breen-Lyles M, Johnson S, Dyer R, Graham R, Chen J, Kashyap P, Farrugia G, Grover M. Serine proteases as luminal mediators of intestinal barrier dysfunction and symptom severity in IBS. Gut. 2020;69:62-73.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 43]  [Cited by in F6Publishing: 53]  [Article Influence: 13.3]  [Reference Citation Analysis (0)]
64.  Roxas JL, Koutsouris A, Bellmeyer A, Tesfay S, Royan S, Falzari K, Harris A, Cheng H, Rhee KJ, Hecht G. Enterohemorrhagic E. coli alters murine intestinal epithelial tight junction protein expression and barrier function in a Shiga toxin independent manner. Lab Invest. 2010;90:1152-1168.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 80]  [Cited by in F6Publishing: 84]  [Article Influence: 6.0]  [Reference Citation Analysis (0)]
65.  Hanevik K, Dizdar V, Langeland N, Hausken T. Development of functional gastrointestinal disorders after Giardia lamblia infection. BMC Gastroenterol. 2009;9:27.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 106]  [Cited by in F6Publishing: 111]  [Article Influence: 7.4]  [Reference Citation Analysis (0)]
66.  Porter CK, Faix DJ, Shiau D, Espiritu J, Espinosa BJ, Riddle MS. Postinfectious gastrointestinal disorders following norovirus outbreaks. Clin Infect Dis. 2012;55:915-922.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 50]  [Cited by in F6Publishing: 52]  [Article Influence: 4.3]  [Reference Citation Analysis (0)]
67.  Zanini B, Ricci C, Bandera F, Caselani F, Magni A, Laronga AM, Lanzini A; San Felice del Benaco Study Investigators. Incidence of post-infectious irritable bowel syndrome and functional intestinal disorders following a water-borne viral gastroenteritis outbreak. Am J Gastroenterol. 2012;107:891-899.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 120]  [Cited by in F6Publishing: 114]  [Article Influence: 9.5]  [Reference Citation Analysis (0)]
68.  Britton GJ, Chen-Liaw A, Cossarini F, Livanos AE, Spindler MP, Plitt T, Eggers J, Mogno I, Gonzalez-Reiche AS, Siu S, Tankelevich M, Grinspan LT, Dixon RE, Jha D, van de Guchte A, Khan Z, Martinez-Delgado G, Amanat F, Hoagland DA, tenOever BR, Dubinsky MC, Merad M, van Bakel H, Krammer F, Bongers G, Mehandru S, Faith JJ. Limited intestinal inflammation despite diarrhea, fecal viral RNA and SARS-CoV-2-specific IgA in patients with acute COVID-19. medRxiv. 2020;.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 24]  [Cited by in F6Publishing: 20]  [Article Influence: 5.0]  [Reference Citation Analysis (0)]
69.  Jena A, Kumar-M P, Singh AK, Sharma V. Fecal calprotectin levels in COVID-19: Lessons from a systematic review on its use in inflammatory bowel disease during the pandemic. Dig Liver Dis. 2021;53:295-297.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 10]  [Cited by in F6Publishing: 10]  [Article Influence: 3.3]  [Reference Citation Analysis (0)]
70.  Oshima T, Siah KTH, Yoshimoto T, Miura K, Tomita T, Fukui H, Miwa H. Impacts of the COVID-19 pandemic on functional dyspepsia and irritable bowel syndrome: A population-based survey. J Gastroenterol Hepatol. 2021;36:1820-1827.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 25]  [Cited by in F6Publishing: 36]  [Article Influence: 12.0]  [Reference Citation Analysis (0)]
71.  Chan WW, Grover M. The COVID-19 Pandemic and Post-Infection Irritable Bowel Syndrome: What Lies Ahead for Gastroenterologists. Clin Gastroenterol Hepatol. 2022;20:2195-2197.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 5]  [Cited by in F6Publishing: 1]  [Article Influence: 0.5]  [Reference Citation Analysis (0)]
72.  Kamp KJ, Levy RL, Munson SA, Heitkemper MM. Impact of COVID-19 on Individuals With Irritable Bowel Syndrome and Comorbid Anxiety and/or Depression. J Clin Gastroenterol. 2022;56:e149-e152.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 11]  [Cited by in F6Publishing: 8]  [Article Influence: 4.0]  [Reference Citation Analysis (0)]
73.  Settanni CR, Ianiro G, Ponziani FR, Bibbò S, Segal JP, Cammarota G, Gasbarrini A. COVID-19 as a trigger of irritable bowel syndrome: A review of potential mechanisms. World J Gastroenterol. 2021;27:7433-7445.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 24]  [Cited by in F6Publishing: 27]  [Article Influence: 9.0]  [Reference Citation Analysis (2)]
74.  Oświęcimska J, Szymlak A, Roczniak W, Girczys-Połedniok K, Kwiecień J. New insights into the pathogenesis and treatment of irritable bowel syndrome. Adv Med Sci. 2017;62:17-30.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 65]  [Cited by in F6Publishing: 55]  [Article Influence: 7.9]  [Reference Citation Analysis (0)]
75.  Bozomitu L, Miron I, Adam Raileanu A, Lupu A, Paduraru G, Marcu FM, Buga AML, Rusu DC, Dragan F, Lupu VV. The Gut Microbiome and Its Implication in the Mucosal Digestive Disorders. Biomedicines. 2022;10.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
76.  Lupu VV, Miron IC, Raileanu AA, Starcea IM, Lupu A, Tarca E, Mocanu A, Buga AML, Lupu V, Fotea S. Difficulties in Adaptation of the Mother and Newborn via Cesarean Section versus Natural Birth-A Narrative Review. Life (Basel). 2023;13:300.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 13]  [Reference Citation Analysis (0)]
77.  Zugravu C, Nanu MI, Moldovanu F, Arghir OC, Mihai CM, Oțelea MR, Cambrea SC. The influence of perinatal education on breastfeeding decision and duration. Int J Child Health Nutr. 2018;7:74-81.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Cited by in F6Publishing: 1]  [Article Influence: 0.2]  [Reference Citation Analysis (0)]
78.  Downs IA, Aroniadis OC, Kelly L, Brandt LJ. Postinfection Irritable Bowel Syndrome: The Links Between Gastroenteritis, Inflammation, the Microbiome, and Functional Disease. J Clin Gastroenterol. 2017;51:869-877.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 20]  [Cited by in F6Publishing: 20]  [Article Influence: 2.9]  [Reference Citation Analysis (0)]
79.  Ghoshal UC. Postinfection Irritable Bowel Syndrome. Gut Liver. 2022;16:331-340.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 11]  [Article Influence: 3.7]  [Reference Citation Analysis (0)]
80.  Barman M, Unold D, Shifley K, Amir E, Hung K, Bos N, Salzman N. Enteric salmonellosis disrupts the microbial ecology of the murine gastrointestinal tract. Infect Immun. 2008;76:907-915.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 315]  [Cited by in F6Publishing: 335]  [Article Influence: 19.7]  [Reference Citation Analysis (0)]
81.  Buret AG, Akierman SV, Feener T, McKnight W, Rioux KP, Beck PL, Wallace JL, Beatty J. Campylobacter Jejuni- or Giardia duodenalis-Mediated Disruptions of Human Intestinal Microbiota Biofilms: Novel Mechanisms Producing Post-Infectious Intestinal Inflammatory Disorders. Gastroenterology. 2013;144:S-309.  [PubMed]  [DOI]  [Cited in This Article: ]
82.  Hsiao A, Ahmed AM, Subramanian S, Griffin NW, Drewry LL, Petri WA Jr, Haque R, Ahmed T, Gordon JI. Members of the human gut microbiota involved in recovery from Vibrio cholerae infection. Nature. 2014;515:423-426.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 311]  [Cited by in F6Publishing: 265]  [Article Influence: 26.5]  [Reference Citation Analysis (0)]
83.  Ma C, Wu X, Nawaz M, Li J, Yu P, Moore JE, Xu J. Molecular characterization of fecal microbiota in patients with viral diarrhea. Curr Microbiol. 2011;63:259-266.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 34]  [Cited by in F6Publishing: 35]  [Article Influence: 2.7]  [Reference Citation Analysis (0)]
84.  Youmans BP, Ajami NJ, Jiang ZD, Campbell F, Wadsworth WD, Petrosino JF, DuPont HL, Highlander SK. Characterization of the human gut microbiome during travelers' diarrhea. Gut Microbes. 2015;6:110-119.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 97]  [Cited by in F6Publishing: 96]  [Article Influence: 10.7]  [Reference Citation Analysis (0)]
85.  Patin NV, Peña-Gonzalez A, Hatt JK, Moe C, Kirby A, Konstantinidis KT. The Role of the Gut Microbiome in Resisting Norovirus Infection as Revealed by a Human Challenge Study. mBio. 2020;11.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 24]  [Cited by in F6Publishing: 23]  [Article Influence: 5.8]  [Reference Citation Analysis (0)]
86.  Nelson AM, Walk ST, Taube S, Taniuchi M, Houpt ER, Wobus CE, Young VB. Disruption of the human gut microbiota following Norovirus infection. PLoS One. 2012;7:e48224.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 92]  [Cited by in F6Publishing: 88]  [Article Influence: 7.3]  [Reference Citation Analysis (0)]
87.  Cheng X, Zhang Y, Li Y, Wu Q, Wu J, Park SK, Guo C, Lu J. Meta-analysis of 16S rRNA microbial data identified alterations of the gut microbiota in COVID-19 patients during the acute and recovery phases. BMC Microbiol. 2022;22:274.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 15]  [Reference Citation Analysis (0)]
88.  Li S, Zhou Y, Yan D, Wan Y. An Update on the Mutual Impact between SARS-CoV-2 Infection and Gut Microbiota. Viruses. 2022;14.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 8]  [Cited by in F6Publishing: 9]  [Article Influence: 4.5]  [Reference Citation Analysis (0)]
89.  Neag MA, Vulturar DM, Gherman D, Burlacu CC, Todea DA, Buzoianu AD. Gastrointestinal microbiota: A predictor of COVID-19 severity? World J Gastroenterol. 2022;28:6328-6344.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 8]  [Cited by in F6Publishing: 8]  [Article Influence: 4.0]  [Reference Citation Analysis (1)]
90.  Mizutani T, Ishizaka A, Koga M, Ikeuchi K, Saito M, Adachi E, Yamayoshi S, Iwatsuki-Horimoto K, Yasuhara A, Kiyono H, Matano T, Suzuki Y, Tsutsumi T, Kawaoka Y, Yotsuyanagi H. Correlation Analysis between Gut Microbiota Alterations and the Cytokine Response in Patients with Coronavirus Disease during Hospitalization. Microbiol Spectr. 2022;10:e0168921.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 6]  [Cited by in F6Publishing: 30]  [Article Influence: 15.0]  [Reference Citation Analysis (0)]
91.  Gu S, Chen Y, Wu Z, Gao H, Lv L, Guo F, Zhang X, Luo R, Huang C, Lu H, Zheng B, Zhang J, Yan R, Zhang H, Jiang H, Xu Q, Guo J, Gong Y, Tang L, Li L. Alterations of the Gut Microbiota in Patients With Coronavirus Disease 2019 or H1N1 Influenza. Clin Infect Dis. 2020;71:2669-2678.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 324]  [Cited by in F6Publishing: 493]  [Article Influence: 164.3]  [Reference Citation Analysis (0)]
92.  Haran JP, Bradley E, Zeamer AL, Cincotta L, Salive MC, Dutta P, Mutaawe S, Anya O, Meza-Segura M, Moormann AM, Ward DV, McCormick BA, Bucci V. Inflammation-type dysbiosis of the oral microbiome associates with the duration of COVID-19 symptoms and long COVID. JCI Insight. 2021;6.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 22]  [Cited by in F6Publishing: 85]  [Article Influence: 28.3]  [Reference Citation Analysis (0)]
93.  Liu Q, Mak JWY, Su Q, Yeoh YK, Lui GC, Ng SSS, Zhang F, Li AYL, Lu W, Hui DS, Chan PK, Chan FKL, Ng SC. Gut microbiota dynamics in a prospective cohort of patients with post-acute COVID-19 syndrome. Gut. 2022;71:544-552.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 186]  [Cited by in F6Publishing: 250]  [Article Influence: 125.0]  [Reference Citation Analysis (0)]
94.  Zuo T, Liu Q, Zhang F, Lui GC, Tso EY, Yeoh YK, Chen Z, Boon SS, Chan FK, Chan PK, Ng SC. Depicting SARS-CoV-2 faecal viral activity in association with gut microbiota composition in patients with COVID-19. Gut. 2021;70:276-284.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 158]  [Cited by in F6Publishing: 243]  [Article Influence: 81.0]  [Reference Citation Analysis (0)]
95.  Zuo T, Zhang F, Lui GCY, Yeoh YK, Li AYL, Zhan H, Wan Y, Chung ACK, Cheung CP, Chen N, Lai CKC, Chen Z, Tso EYK, Fung KSC, Chan V, Ling L, Joynt G, Hui DSC, Chan FKL, Chan PKS, Ng SC. Alterations in Gut Microbiota of Patients With COVID-19 During Time of Hospitalization. Gastroenterology. 2020;159:944-955.e8.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 739]  [Cited by in F6Publishing: 916]  [Article Influence: 229.0]  [Reference Citation Analysis (0)]
96.  Yeoh YK, Zuo T, Lui GC, Zhang F, Liu Q, Li AY, Chung AC, Cheung CP, Tso EY, Fung KS, Chan V, Ling L, Joynt G, Hui DS, Chow KM, Ng SSS, Li TC, Ng RW, Yip TC, Wong GL, Chan FK, Wong CK, Chan PK, Ng SC. Gut microbiota composition reflects disease severity and dysfunctional immune responses in patients with COVID-19. Gut. 2021;70:698-706.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 521]  [Cited by in F6Publishing: 709]  [Article Influence: 236.3]  [Reference Citation Analysis (0)]
97.  Budden KF, Gellatly SL, Wood DL, Cooper MA, Morrison M, Hugenholtz P, Hansbro PM. Emerging pathogenic links between microbiota and the gut-lung axis. Nat Rev Microbiol. 2017;15:55-63.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 622]  [Cited by in F6Publishing: 836]  [Article Influence: 104.5]  [Reference Citation Analysis (0)]
98.  Dicksved J, Ellström P, Engstrand L, Rautelin H. Susceptibility to Campylobacter infection is associated with the species composition of the human fecal microbiota. mBio. 2014;5:e01212-e01214.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 57]  [Cited by in F6Publishing: 60]  [Article Influence: 6.0]  [Reference Citation Analysis (0)]
99.  Sundin J, Rangel I, Fuentes S, Heikamp-de Jong I, Hultgren-Hörnquist E, de Vos WM, Brummer RJ. Altered faecal and mucosal microbial composition in post-infectious irritable bowel syndrome patients correlates with mucosal lymphocyte phenotypes and psychological distress. Aliment Pharmacol Ther. 2015;41:342-351.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 108]  [Cited by in F6Publishing: 96]  [Article Influence: 10.7]  [Reference Citation Analysis (0)]
100.  Mari A, Abu Baker F, Mahamid M, Sbeit W, Khoury T. The Evolving Role of Gut Microbiota in the Management of Irritable Bowel Syndrome: An Overview of the Current Knowledge. J Clin Med. 2020;9.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 21]  [Cited by in F6Publishing: 24]  [Article Influence: 6.0]  [Reference Citation Analysis (0)]
101.  Hill C, Guarner F, Reid G, Gibson GR, Merenstein DJ, Pot B, Morelli L, Canani RB, Flint HJ, Salminen S, Calder PC, Sanders ME. Expert consensus document. The International Scientific Association for Probiotics and Prebiotics consensus statement on the scope and appropriate use of the term probiotic. Nat Rev Gastroenterol Hepatol. 2014;11:506-514.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4055]  [Cited by in F6Publishing: 4619]  [Article Influence: 461.9]  [Reference Citation Analysis (2)]
102.  Compare D, Rocco A, Coccoli P, Angrisani D, Sgamato C, Iovine B, Salvatore U, Nardone G. Lactobacillus casei DG and its postbiotic reduce the inflammatory mucosal response: an ex-vivo organ culture model of post-infectious irritable bowel syndrome. BMC Gastroenterol. 2017;17:53.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 58]  [Cited by in F6Publishing: 67]  [Article Influence: 9.6]  [Reference Citation Analysis (0)]
103.  Hong KB, Seo H, Lee JS, Park Y. Effects of probiotic supplementation on post-infectious irritable bowel syndrome in rodent model. BMC Complement Altern Med. 2019;19:195.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 12]  [Cited by in F6Publishing: 13]  [Article Influence: 2.6]  [Reference Citation Analysis (0)]
104.  Abbas Z, Yakoob J, Jafri W, Ahmad Z, Azam Z, Usman MW, Shamim S, Islam M. Cytokine and clinical response to Saccharomyces boulardii therapy in diarrhea-dominant irritable bowel syndrome: a randomized trial. Eur J Gastroenterol Hepatol. 2014;26:630-639.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 55]  [Cited by in F6Publishing: 58]  [Article Influence: 5.8]  [Reference Citation Analysis (0)]
105.  Lawenko RMA, Lee YY, Nurfadhilah Y, Yaacob N, Mohammad WMZW, Liong MT. The role of gut dysbiosis and probiotics in persistent abdominal pain following a major flood disaster. J Gastroenterol Hepatol. 2016;31:131.  [PubMed]  [DOI]  [Cited in This Article: ]
106.  Lee YY, Annamalai C, Rao SSC. Post-Infectious Irritable Bowel Syndrome. Curr Gastroenterol Rep. 2017;19:56.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 30]  [Cited by in F6Publishing: 27]  [Article Influence: 3.9]  [Reference Citation Analysis (0)]
107.  Cao YN, Feng LJ, Liu YY, Jiang K, Zhang MJ, Gu YX, Wang BM, Gao J, Wang ZL, Wang YM. Effect of Lactobacillus rhamnosus GG supernatant on serotonin transporter expression in rats with post-infectious irritable bowel syndrome. World J Gastroenterol. 2018;24:338-350.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 33]  [Cited by in F6Publishing: 30]  [Article Influence: 5.0]  [Reference Citation Analysis (0)]
108.  Chen YM, Li Y, Wang X, Wang ZL, Hou JJ, Su S, Zhong WL, Xu X, Zhang J, Wang BM, Wang YM. Effect of Bacillus subtilis, Enterococcus faecium, and Enterococcus faecalis supernatants on serotonin transporter expression in cells and tissues. World J Gastroenterol. 2022;28:532-546.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 2]  [Cited by in F6Publishing: 2]  [Article Influence: 1.0]  [Reference Citation Analysis (2)]
109.  Zhang F, Lau RI, Liu Q, Su Q, Chan FKL, Ng SC. Gut microbiota in COVID-19: key microbial changes, potential mechanisms and clinical applications. Nat Rev Gastroenterol Hepatol. 2023;20:323-337.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 32]  [Cited by in F6Publishing: 59]  [Article Influence: 59.0]  [Reference Citation Analysis (0)]
110.  Tkach S, Dorofeyev A, Kuzenko I, Sulaieva O, Falalyeyeva T, Kobyliak N. Fecal microbiota transplantation in patients with post-infectious irritable bowel syndrome: A randomized, clinical trial. Front Med (Lausanne). 2022;9:994911.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
111.  Liu X, Li Y, Wu K, Shi Y, Chen M. Fecal Microbiota Transplantation as Therapy for Treatment of Active Ulcerative Colitis: A Systematic Review and Meta-Analysis. Gastroenterol Res Pract. 2021;2021:6612970.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 18]  [Cited by in F6Publishing: 16]  [Article Influence: 5.3]  [Reference Citation Analysis (0)]
112.  Liu F, Ye S, Zhu X, He X, Wang S, Li Y, Lin J, Wang J, Lin Y, Ren X, Deng Z. Gastrointestinal disturbance and effect of fecal microbiota transplantation in discharged COVID-19 patients. J Med Case Rep. 2021;15:60.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 42]  [Cited by in F6Publishing: 46]  [Article Influence: 15.3]  [Reference Citation Analysis (0)]
113.  Jin Y, Ren X, Li G, Li Y, Zhang L, Wang H, Qian W, Hou X. Beneficial effects of Rifaximin in post-infectious irritable bowel syndrome mouse model beyond gut microbiota. J Gastroenterol Hepatol. 2018;33:443-452.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 21]  [Cited by in F6Publishing: 21]  [Article Influence: 3.5]  [Reference Citation Analysis (0)]
114.  Harris LA. Rifaximin for Irritable Bowel Syndrome (IBS) in Gulf War Veterans: Losing the Battle but Winning the War? Dig Dis Sci. 2019;64:609-610.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 3]  [Article Influence: 0.6]  [Reference Citation Analysis (0)]
115.  Tuteja AK, Talley NJ, Stoddard GJ, Verne GN. Double-Blind Placebo-Controlled Study of Rifaximin and Lactulose Hydrogen Breath Test in Gulf War Veterans with Irritable Bowel Syndrome. Dig Dis Sci. 2019;64:838-845.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 18]  [Cited by in F6Publishing: 17]  [Article Influence: 3.4]  [Reference Citation Analysis (0)]
116.  Lam C, Tan W, Leighton M, Hastings M, Lingaya M, Falcone Y, Zhou X, Xu L, Whorwell P, Walls AF, Zaitoun A, Montgomery A, Spiller R. A mechanistic multicentre, parallel group, randomised placebo-controlled trial of mesalazine for the treatment of IBS with diarrhoea (IBS-D). Gut. 2016;65:91-99.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 61]  [Cited by in F6Publishing: 69]  [Article Influence: 8.6]  [Reference Citation Analysis (0)]
117.  Bafutto M, Almeida JR, Leite NV, Oliveira EC, Gabriel-Neto S, Rezende-Filho J. Treatment of postinfectious irritable bowel syndrome and noninfective irritable bowel syndrome with mesalazine. Arq Gastroenterol. 2011;48:36-40.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 15]  [Cited by in F6Publishing: 17]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
118.  Tuteja AK, Fang JC, Al-Suqi M, Stoddard GJ, Hale DC. Double-blind placebo-controlled study of mesalamine in post-infective irritable bowel syndrome--a pilot study. Scand J Gastroenterol. 2012;47:1159-1164.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 28]  [Cited by in F6Publishing: 29]  [Article Influence: 2.4]  [Reference Citation Analysis (0)]
119.  Andresen V, Löwe B, Broicher W, Riegel B, Fraedrich K, von Wulffen M, Gappmayer K, Wegscheider K, Treszl A, Rose M, Layer P, Lohse AW. Post-infectious irritable bowel syndrome (PI-IBS) after infection with Shiga-like toxin-producing Escherichia coli (STEC) O104:H4: A cohort study with prospective follow-up. United European Gastroenterol J. 2016;4:121-131.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 27]  [Cited by in F6Publishing: 26]  [Article Influence: 3.3]  [Reference Citation Analysis (0)]
120.  Dunlop SP, Jenkins D, Neal KR, Naesdal J, Borgaonker M, Collins SM, Spiller RC. Randomized, double-blind, placebo-controlled trial of prednisolone in post-infectious irritable bowel syndrome. Aliment Pharmacol Ther. 2003;18:77-84.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 122]  [Cited by in F6Publishing: 110]  [Article Influence: 5.2]  [Reference Citation Analysis (0)]
121.  Barkun AN, Love J, Gould M, Pluta H, Steinhart H. Bile acid malabsorption in chronic diarrhea: pathophysiology and treatment. Can J Gastroenterol. 2013;27:653-659.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 56]  [Cited by in F6Publishing: 60]  [Article Influence: 6.0]  [Reference Citation Analysis (0)]