The gut microbiome comprises a vast community of microbes inhabiting the human alimentary canal, playing a crucial role in various physiological functions. These microbes generally live in harmony with the host; however, when dysbiosis occurs, it can contribute to the pathogenesis of diseases, including osteoporosis. Osteoporosis, a systemic skeletal disease characterized by reduced bone mass and increased fracture risk, has attracted significant research attention concerning the role of gut microbes in its development. Advances in molecular biology have highlighted the influence of gut microbiota on osteoporosis through mechanisms involving immunoregulation, modulation of the gut-brain axis, and regulation of the intestinal barrier and nutrient absorption. These microbes can enhance bone mass by inhibiting osteoclast differentiation, inducing apoptosis, reducing bone resorption, and promoting osteoblast proliferation and maturation. Despite these promising findings, the therapeutic effectiveness of targeting gut microbes in osteoporosis requires further investigation. Notably, gut microbiota has been increasingly studied for their potential in early diagnosis, intervention, and as an adjunct therapy for osteoporosis, suggesting a growing utility in improving bone health. Further research is essential to fully elucidate the therapeutic potential and clinical application of gut microbiome modulation in the management of osteoporosis.

Phage therapy is an effective strategy to combat multidrug resistance in bacteria and has been increasingly utilized to protect animals from bacterial infections. This study involved the isolation and purification of a novel myoviruses phage, vB_AceP_PAc, from a drug-resistant bacterial strain Aeromonas caviae. Genome sequence analysis based on nucleotide sequences revealed that vB_AceP_PAc shared significant similarity with the genomes of 10 other Aeromonas phages, with the highest coverage rate of 52% with phiA047. Intraperitoneal injection of 1 × 10⁷ CFU/mL (100 µL/mouse) A. caviae AC-CY resulted in diarrhea in mice three days later. At this time, oral administration of 1 × 109 PFU/mL (100 µL/mouse) vB_AceP_PAc effectively alleviated the diarrhea induced by Pseudomonas aeruginosa infection in the mice. Furthermore, oral administration of 1 × 109 PFU/ml vB_AceP_PAc (100 µl/mouse) in healthy mice significantly reduced inflammatory cytokine levels, increased tight junction molecule levels, and improved intestinal barrier function. Moreover, the consumption of vB_AceP_PAc by health mice led to a significant increase in the abundance of Lactobacillaceae in the gut, while the expression of CD3+CD4+/CD3+CD8+ was minimally affected. Overall, the findings of this study confirmed the promising potential of bacteriophage vB_AceP_PAc in treating diarrhea caused by A. caviae.

Heart failure (HF) is a leading cause of death worldwide. We have shown that pressure overload (PO)-induced inflammatory cell recruitment leads to heart failure in IL-10 knockout (KO) mice. However, it is unclear whether PO-induced inflammatory cells also target the gut mucosa, causing gut dysbiosis and leakage. We hypothesized that transverse aortic constriction (TAC) exacerbates immune cell homing to the gut (small intestine and colon), promoting dysbiosis and gut leakage in IL-10 KO mice. HF was induced in 8- to 10-wk-old C57BL/6J wild-type (WT) and B6.129P2-Il10tm1Cgn/J mutant (IL-10 KO) male and female mice by TAC and cardiac function was measured using visual sonics VEVO 3100. Fourteen days post-TAC, levels of monocytes, macrophages, neutrophils, and proinflammatory cytokines were measured in blood and gut. Gut dysbiosis was assessed via 16S rRNA sequencing in feces at 56 days post-TAC. IL-10 KO mice showed worsened cardiac dysfunction post-TAC. TAC worsened monocytes, and neutrophils infiltration in systemic circulation and facilitated their homing to the gut in IL-10 KO mice. Intriguingly, proinflammatory cytokines level was increased in blood, and gut of IL-10 KO mice following TAC. Furthermore, IL-10 expression was reduced in the colon of WT mice post-TAC. Moreover, TAC exacerbated gut dysbiosis in IL-10 KO mice. Finally, an impaired intestinal permeability was noted in IL-10 KO mice post-TAC. In conclusion, TAC-induced systemic inflammation leads to gut dysbiosis and impaired gut permeability in IL-10 KO mice, indicating IL-10's potential role in regulating intestinal integrity and microbiota balance during heart failure.NEW & NOTEWORTHY IL-10, crucial for systemic inflammation regulation and gut mucosal homeostasis, was investigated using IL-10 knockout (KO) mice. Exacerbated gut inflammation was observed post-transverse aortic constriction (TAC) in IL-10-depleted mice, whereas wild-type (WT) mice showed reduced IL-10 gene expression in colon and ileum. TAC induced gut dysbiosis and leakage in IL-10 KO mice, suggesting a link between enhanced inflammatory signaling in heart failure and multi-organ damage via gut dysbiosis and leakage.

Preeclampsia (PE) is a life-threatening hypertensive disorder of pregnancy with an incidence rate of up to 8% worldwide. However, the complete pathogenesis is still unknown. Obesity increases the risk of developing PE threefold. To better understand the relationship of maternal risk factors, the BPH/5 mouse was described as a model of superimposed PE. Previous research demonstrated that adult BPH/5 female mice have an adverse cardiometabolic phenotype characterized by hypertension, obesity with increased white adipose tissue, and dyslipidemia, exaggerated by pregnancy. We hypothesize that BPH/5 mice have gut dysbiosis characterized by changes in alpha and beta diversity of bacterial community structure as well as perturbed short-chain fatty acids (SCFAs) compared with controls in pregnancy. Fecal samples were used for Illumina sequencing of 16S v4 rRNA amplicons. Microbial community composition of the pregnant BPH/5 mice compared with C57 controls was different using permutational multivariate analysis of variance (PERMANOVA) with Bray-Curtis dissimilarity. Alpha diversity was increased in pregnant BPH/5 dams compared with controls. Alistipes and Helicobacter were increased, whereas Bacteroides, Lactobacillus, Parasutterella, and Parabacteroides were decreased compared with controls. Fecal SCFAs were not different between groups, but BPH/5 serum acetic and butyric acids were decreased, whereas isobutyric and isovaleric acids were increased specifically in pregnancy. BPH/5 pregnant colons had decreased expression of free fatty acid receptor, GPR41. In conclusion, the BPH/5 maternal fecal microbiome demonstrates microbial dysbiosis characterized by community structure and diversity changes before and after the onset of pregnancy. Gut dysbiosis may be a key mechanism linking SCFA signaling and obesity to the BPH/5 PE-like phenotype.NEW & NOTEWORTHY This is the first time the pregnant fecal microbiome has been identified in the BPH/5 spontaneous mouse model of superimposed PE. Community composition changed with the onset of pregnancy in this model. BPH/5 showed an altered colonic signaling with decreased GPR41 expression, suggesting that gut dysbiosis may link SCFA signaling to the PE phenotype. This data highlights the importance of the maternal obesogenic gut microbiome in pregnancy.

Antibiotic overuse is driving a global rise in antibiotic resistance, highlighting the need for robust antimicrobial stewardship (AMS) initiatives to improve prescription practices. While antimicrobials are essential for treating sepsis and preventing surgical site infections (SSIs), they can inadvertently disrupt the gut microbiota, leading to postoperative complications. Treatment methods vary widely across nations due to differences in drug choice, dosage, and therapy duration, affecting antibiotic resistance rates, which can reach up to 51% in some countries. In Romania and the Republic of Moldova, healthcare practices for surgical antibiotic prophylaxis differ significantly despite similarities in genetics, culture, and diet. Romania's stricter healthcare regulations result in more standardized antibiotic protocols, whereas Moldova's limited healthcare funding leads to less consistent practices and greater variability in treatment outcomes.

This study presents the results of a prospective cross-border investigation involving 86 colorectal cancer patients from major oncological hospitals in Romania and Moldova. We analyzed fecal samples collected from patients before and 7 days post-antibiotic treatment, focusing on the V3-V4 region of the 16S rRNA gene.

Our findings indicate that inconsistent antibiotic prophylaxis policies-varying in type, dosage, or therapy duration-significantly impacted the gut microbiota and led to more frequent dysbiosis compared to stricter prophylactic antibiotic practices (single dose, single product, limited time).

We emphasize the need for standardized antibiotic prophylaxis protocols to minimize dysbiosis and its associated risks, promoting more effective antimicrobial use, particularly in low- and middle-income countries (LMICs).

Studies conducted so far have shown that nano- and microplastic may disturb the intestinal microenvironment by interacting with the intestinal epithelium and the gut microbiota. Depending on the research model used, the effect on the microbiome is different-an increase or decrease in selected taxa resulting in the development of dysbiosis. Dysbiosis may be associated with intestinal inflammation, development of mental disorders or diabetes. The aim of the study was to analyze the intestinal microbiome in 15 gilts divided into 3 research groups (n = 5; control group, receiving micropartices at a dose 0.1 g/day (LD) and 1 g/day (HD)). Feaces were collected before and after 28 days of exposure to PET microplastics. The analysis of the intestinal microbiome was performed using next-generation sequencing. Alpha and beta diversity indices were compared, showing, that repetition affected only the abundance indices in the control and LD groups, but not in the HD group. The relationships between the number of reads at the phylum, genus and species level and the microplastic dose were calculated using statistical methods (r-Pearson correlation, generalized regression model, analysis of variance). The statistical analysis revealed, that populations of Family XIII AD3011 group, Coprococcus, V9D2013 group, UCG-010 and Sphaerochaeta increased with increasing MP-PET dose. The above-mentioned taxa are mainly responsible for the production of short-chain fatty acids (SCFA). It may be assumed, that SCFA are one of the mechanisms involved in the response to oral exposure to MP-PET.

Gestational diabetes mellitus (GDM), a severe pregnancy disorder, is a temporary form of diabetes that occurs during gestation. Astragaloside IV (AS IV), a natural and effective composition of Astragalus membranaceus, shows pharmacological effects against diabetes. On the contrary, the effects of AS IV on GDM development are still not clear. This study aims to investigate the role of AS IV in alleviating GDM in rats and determine whether AS IV exerts its anti-GDM properties through the regulation of gut microbiota and metabolite modulation.

There were six pregnant SD rats in each of the four groups. First, the GDM model was induced by the streptozotocin (STZ, 45 mg/kg) injection on gestational days (GDs) 1-4, and AS IV intervention (10 mg/kg/d) was administered from 6 days before pregnancy until delivery. The measurements of relevant indicators pertaining to GDM symptoms and reproductive outcomes, along with the 16S rRNA sequencing data and LC-MS-based metabolomic profiles, were assessed across all groups.

After the 25-day intervention, the GDM model + AS IV group showed significantly decreased fasting blood glucose levels (p = 0.0003), mean insulin levels (p = 0.0001), and insulin resistance index (p = 0.0001). AS IV treatment also decreased the malformation rate (p = 0.0373) and increased the average fetal weight (p = 0.0020) of GDM rats. Compared to the control rats, GDM rats showed a significantly higher abundance of Blautia and Anaerobiospirillum. However, the dramatically elevated abundance of these microorganisms was markedly decreased by AS IV treatment. In contrast, compared to GDM rats without treatment, GDM rats treated with AS IV showed a significantly higher abundance of bacteria (p < 0.05), such as Methanobrevibacter, Dubosiella, and Romboutsia, which are beneficial to the rats. Additionally, we observed dramatically elevated production of metabolites, such as N-acetyl-l-leucine and lithocholic acid, after AS IV treatment through metabolomics analysis (p < 0.05). Furthermore, significant associations between most genera of gut bacteria and the altered levels of the metabolites connected to gut microbiota were also discovered.

Our study demonstrated that AS IV could be an effective nutritional intervention strategy for targeting gut microbiota and metabolome profiles in GDM and provided experimental evidence supporting the use of AS IV to treat GDM.

The study aimed to evaluate the effects of increasing levels of a microencapsulated blend of botanicals (MBB) on the intestinal health and growth performance of nursery pigs challenged with F18+E. coli. Sixty-four nursery pigs (6.8 ± 0.3 kg) were assigned to 4 dietary treatments in a randomized complete block design, with initial body weight and sex as blocks, and fed for 28 d in 3 phases. Treatments were a basal diet fed to pigs without F18+E. coli challenge (NC) and 3 levels of MBB (0.0%, 0.1%, and 0.2%) in pigs challenged with F18+E. coli. On day 7 of the study, pigs in the challenged group were orally inoculated with F18+E. coli (1.5 × 1010 CFU). On days 7 and 21 post-challenge, pigs were euthanized to collect jejunal tissues and mucosa. Compared to the NC, 0.0% MBB increased (P < 0.05) relative abundance (RA) of Staphylococcus saprophyticus and reduced (P < 0.05) Streptococcus parasuis at days 7 and 21 post-challenge, respectively. Increasing levels of MBB decreased (linear: P < 0.05) RA of S. saprophyticus on day 7 post-challenge. Compared to the NC, 0.0% MBB increased (P < 0.05) jejunal NOD2 and IL-6 expression and decreased (P < 0.05) ZO-1 on day 7 post-challenge. Compared to the NC, 0.0% MBB decreased (P < 0.05) jejunal IL-6, IL-8, and TNF-α and increased (P < 0.05) IgG on day 21 post-challenge. Increasing levels of MBB increased OCLN (linear: P < 0.05) and ZO-1 (linear and quadratic: P < 0.05) on day 7 post-challenge and decreased toll-like receptor 4 (TLR4; linear and quadratic: P < 0.05). Compared to the NC, 0.0% MBB decreased (P < 0.05) Ki-67+ on day 7 post-challenge. Increasing levels of MBB increased (linear: P < 0.05) Ki-67+ on day 7 post-challenge and villus height (VH):CD on d 21 post-challenge. In the overall period, compared to the NC, 0.0% MBB decreased (P < 0.05) average daily gain. Increasing daily MBB intake linearly increased OCLN on day 7 and VH:CD on day 21, and reduced TLR4 and IL-8 on day 21 post-challenge, but exhibiting quadratic effects (P < 0.05) on ZO-1 (optimal at 0.12% of MBB), IgG (optimal at 0.14% of MBB), and G:F during days 7 to 20 and days 7 to 28 (optimal at 0.22% and 0.10% of MBB, respectively). In conclusion, F18+E. coli challenge negatively modulated the jejunal mucosal microbiota and reduced intestinal morphology and growth of nursery pigs. Supplementation of MBB at 0.10% to 0.14% provided optimal mitigation of the impacts of F18+E. coli challenge on humoral immunity, intestinal integrity, jejunal morphology, and feed efficiency of pigs.

The human body constitutes a living environment for trillions of microorganisms, which establish the microbiome and, the largest population among them, reside within the gastrointestinal tract, establishing the gut microbiota. The term "gut microbiota" refers to a set of many microorganisms [mainly bacteria], which live symbiotically within the human host. The term "microbiome" means the collective genomic content of these microorganisms. The number of bacterial cells within the gut microbiota exceeds the host's cells; collectively and their genes quantitatively surpass the host's genes. Immense scientific research into the nature and function of the gut microbiota is unraveling its roles in certain human health activities such as metabolic, physiology, and immune activities and also in pathologic states and diseases. Interestingly, the microbiota, a dynamic ecosystem, inhabits a particular environment such as the human mouth or gut. Human microbiota can evolve and even adapt to the host's unique features such as eating habits, genetic makeup, underlying diseases, and even personalized habits. In the past decade, biologists and bioinformaticians have concentrated their research effort on the potential roles of the gut microbiome in the development of human diseases, particularly immune-mediated diseases and colorectal cancer, and have initiated the assessment of the impact of the gut microbiome on the host genome. In the present chapter, we focus on the biological features of gut microbiota, its physiology as a biological factory, and its impacts on the host's health and disease status.

Major depressive disorder (MDD) represents a complex and challenging mental health condition with multifaceted etiology. Recent research exploring the gut-brain axis has shed light on the potential influence of gut microbiota on mental health, offering novel avenues for therapeutic intervention. This paper reviews current evidence on the role of prebiotics and probiotics in the context of MDD treatment. Clinical studies assessing the effects of prebiotic and probiotic interventions have demonstrated promising results, showcasing improvements in depression symptoms and metabolic parameters in certain populations. Notably, prebiotics and probiotics have shown the capacity to modulate inflammatory markers, cortisol levels, and neurotransmitter pathways linked to MDD. However, existing research presents varied outcomes, underscoring the need for further investigation into specific microbial strains, dosage optimization, and long-term effects. Future research should aim at refining personalized interventions, elucidating mechanisms of action, and establishing standardized protocols to integrate these interventions into clinical practice. While prebiotics and probiotics offer potential adjunctive therapies for MDD, continued interdisciplinary efforts are vital to harnessing their full therapeutic potential and reshaping the landscape of depression treatment paradigms.

Previous studies have suggested a potential association between the gut microbiota and arthritis. However, the causal links between the gut microbiota and various types of arthritis, as well as the potential mediating role of inflammatory proteins, remain unclear. Mendelian randomization was used to explore the causal relationships between gut microbiota, inflammatory proteins, and various forms of arthritis (osteoarthritis, rheumatoid and psoriatic arthritis, and ankylosing spondylitis [AS]). The inverse variance-weighted method was the primary analytical approach used. Furthermore, we examined the mediating role of inflammatory proteins in the pathway linking the gut microbiota to arthritis. Sensitivity analyses were performed to verify the robustness of the findings, and enrichment analyses were conducted to investigate the biological functions and pathways involved. We identified 11 positive and 14 negative causal effects linking the genetic liability of the gut microbiota to arthritis. Similarly, 9 positive and 8 negative causal effects between inflammatory proteins and arthritis were identified. Notably, an increased abundance of the order Bacillales (odds ratio [OR] = 1.199, 95% confidence interval [CI] = 1.030-1.394, P = 0.019) and higher interleukin-7 levels (OR = 1.322, 95% CI = 1.004-1.741, P = 0.046) significantly elevated the risk of AS. Furthermore, interleukin-7 mediated 13.8% of the effect caused by the order Bacillales, with a mediation effect size of β = 0.025 (95% CI = 0.001-0.064). Sensitivity and supplementary analyses revealed no significant evidence of horizontal pleiotropy or heterogeneity. Overall, our findings demonstrate causal links between the gut microbiota, inflammatory proteins, and four arthritis types, highlighting the gut microbiota as a potential therapeutic target. Crucially, interleukin-7 not only strongly correlated with AS but also partially mediated the effect exerted by the gut microbiota on AS, suggesting that managing the gut microbiota to modulate inflammatory proteins could serve as an effective therapeutic strategy for arthritis.

This review explores the complex relationship between gut dysbiosis and hematological malignancies, focusing on graft-versus-host disease (GvHD) in allogeneic hematopoietic stem cell transplantation (allo-HSCT) recipients. We discuss how alterations in microbial diversity and composition can influence disease development, progression, and treatment outcomes in blood cancers. The mechanisms by which the gut microbiota impacts these conditions are examined, including modulation of immune responses, production of metabolites, and effects on intestinal barrier function. Recent advances in microbiome-based therapies for treating and preventing GvHD are highlighted, with emphasis on full ecosystem standardized donor-derived products. Overall, this review underscores the growing importance of microbiome research in hematology-oncology and its potential to complement existing treatments and improve outcomes for thousands of patients worldwide.

Colorectal cancer (CRC) ranks among the most prevalent malignant tumors worldwide, with a multifactorial etiology encompassing genetic, environmental, and life-style factors, as well as the intestinal microbiota and its metabolome. These risk factors often work together in specific groups of patients, influencing how CRC develops and progresses. Importantly, alterations in the gut microbiota act as a critical nexus in this interplay, significantly affecting susceptibility to CRC. This review highlights recent insights into unmodifiable and modifiable risk factors for CRC and how they might interact with the gut microbiota and its metabolome. Understanding the mechanisms of these interactions will help us develop targeted, precision-medicine strategies that can adjust the composition of the gut microbiota to meet individual health needs, preventing or treating CRC more effectively.

Gastrointestinal (GI) infection by intestinal pathogens poses great threats to human health, and the therapeutic use of antibiotics has reached a bottleneck due to drug resistance. The developments of antimicrobial peptides produced by beneficial bacteria have drawn attention by virtue of effective, safe, and not prone to developing resistance. Though bacteriocin as antimicrobial agent in gut infection has been intensively investigated and reviewed, reviews on that of bacteriocin-producing beneficial microbes are very rare. It is important to explicitly state the prospect of bacteriocin-producing microbes in prevention of gastrointestinal infection towards their application in host. This review discusses the potential of gut as an appropriate resource for mining targeted bacteriocin-producing microbes. Then, host-related factors affecting the bacteriocin production and activity of bacteriocin-producing microbes in the gut are summarized. Accordingly, the multiple mechanisms (direct inhibition and indirect inhibition) behind the preventive effects of bacteriocin-producing microbes on gut infection are discussed. Finally, we propose several targeted strategies for the manipulation of bacteriocin-producing beneficial microbes to improve their performance in antimicrobial outcomes. We anticipate an upcoming emergence of developments and applications of bacteriocin-producing beneficial microbes as antimicrobial agent in gut infection induced by pathogenic bacteria.

The disturbed gut microbiota is a key factor in activating the aflatoxin B1 (AFB1)-induced liver pyroptosis by promoting inflammatory hepatic injury; however, the pathogen associated molecular pattern (PAMP) from disturbed gut microbiota and its mechanism in activating liver pyroptosis remain undefined. By transplanting AFB1-originated fecal microbiota and sterile fecal microbial metabolites filtrate, we determined the association of PAMP in AFB1-induced liver pyroptosis. Notably, AFB1-originated sterile fecal microbial metabolites filtrate were more active in triggering liver pyroptosis in mice, as compared to parental fecal microbiota. This result supported a critical role of the metabolic homeostasis of gut microbiota in AFB1-induced liver pyroptosis, rather than an injurious response to direct exposure of AFB1 in liver. Among the gut-microbial metabolites, pipecolic acid and norepinephrine were proposed to bind TLR4 and NLRP3, the upstream proteins of pyroptosis signaling pathway. Besides, the activations of TLR4 and NLRP3 were linearly correlated with the concentrations of pipecolic acid and norepinephrine in the serum of mice. In silenced expression of TLR4 and NLRP3 in HepG2 cells, pipecolic acid or norepinephrine did not able to activate hepatocyte pyroptosis. These results demonstrated the necessity of gut microbial metabolism in sustaining liver homeostasis, as well as the potential to provide new insights into targeted intervention for AFB1 hepatotoxicity.

The intestinal wall is a selectively permeable barrier between the content of the intestinal lumen and the internal environment of the body. Disturbances of intestinal wall permeability can potentially lead to unwanted activation of the enteric immune system due to excessive contact with gut microbiota and its components, and the development of endotoxemia, when the level of bacterial lipopolysaccharides increases in the blood, causing chronic low-intensity inflammation. In this review, the following aspects are covered: the structure of the intestinal wall barrier; the influence of the gut microbiota on the permeability of the intestinal wall via the regulation of functioning of tight junction proteins, synthesis/degradation of mucus and antioxidant effects; the molecular mechanisms of activation of the pro-inflammatory response caused by bacterial invasion through the TLR4-induced TIRAP/MyD88 and TRAM/TRIF signaling cascades; the influence of nutrition on intestinal permeability, and the influence of exercise with an emphasis on exercise-induced heat stress and hypoxia. Overall, this review provides some insight into how to prevent excessive intestinal barrier permeability and the associated inflammatory processes involved in many if not most pathologies. Some diets and physical exercise are supposed to be non-pharmacological approaches to maintain the integrity of intestinal barrier function and provide its efficient operation. However, at an early age, the increased intestinal permeability has a hormetic effect and contributes to the development of the immune system.

Urinary tract infection (UTI) is a well-known bacterial infection posing serious health problem in children. A retrospective study was conducted to explore the uropathogen and its antibiotic resistance in children with UTI. Data of urine culture and antimicrobial susceptibility test was collected. Consequently, 840 children were included. The overall culture-positive UTI was 458 (54.52 %) with Escherichia coli 166 (36.24 %), followed by Enterococcus faecalis 59 (12.88 %), Enterococcus faecium 70 (15.28 %) and others. They were highly resistant to the most commonly used antibiotics. In 694 children with complicated UTI, there were 8 children with fungal infection. Multiple drug resistance (MDR) was recorded in 315 (80.98 %). The overall proportion of Extended Spectrum β-Lactamase (ESβL) production was 25 (6.43 %). In 146 children with simple UTI, MDR were also detected in 47 (77.05 %). There were 6 (9.84 %) positive for ESβL production. Our study found that complicated UTI was relatively common. Escherichia coli was the most prevalent isolate, followed by Enterococcus faecium and Enterococcus faecalis. These organisms were highly resistant to the most commonly used antibiotics. Relatively high prevalence of MDR and low ESβL-producing organisms were observed.

The present treatments for bronchiectasis, which is defined by pathological dilatation of the airways, are confined to symptom relief and minimizing exacerbations. The condition is becoming more common worldwide. Since the disease's pathophysiology is not entirely well understood, developing novel treatments is critically important. The interplay of chronic infection, inflammation, and compromised mucociliary clearance, which results in structural alterations and the emergence of new infection, is most likely responsible for the progression of bronchiectasis. Other than treating bronchiectasis caused by cystic fibrosis, there are no approved treatments. Understanding the involvement of the microbiome in this disease is crucial, the microbiome is defined as the collective genetic material of all bacteria in an environment. In clinical practice, bacteria in the lungs have been studied using cultures; however, in recent years, researchers use next-generation sequencing methods, such as 16S rRNA sequencing. Although the microbiome in bronchiectasis has not been entirely investigated, what is known about it suggests that Haemophilus, Pseudomonas and Streptococcus dominate the lung bacterial ecosystems, they present significant intraindividual stability and interindividual heterogeneity. Pseudomonas and Haemophilus-dominated microbiomes have been linked to more severe diseases and frequent exacerbations, however additional research is required to fully comprehend the role of microbiome in the evolution of bronchiectasis. This review discusses recent findings on the lung microbiota and its association with bronchiectasis.

The recent rise in hand sanitizer use due to the COVID-19 pandemic has had a beneficial impact on stopping the spread of disease, but the potential negative implications of its overuse on the body and the microbiome have yet to be thoroughly reviewed. Epidermal layers absorb hand sanitizer from direct application to the skin, making them some of the most susceptible cells to the adverse effects of overuse. The increased usage of hand sanitizer can affect the variation, quantity, and diversity of the skin microflora, leading to conditions such as eczema, atopic dermatitis, and even systemic toxicity due to colonization of the skin with pathogenic bacteria. Due to the close-knit relationship between the skin and gut, the gastrointestinal system can also incur disruptions due to the negative effects on the skin as a result of excessive hand sanitizer use, leading to gut dysbiosis. Additionally, the accidental ingestion of hand sanitizer, and its abuse or misuse, can be toxic and lead to alcohol poisoning, which is an issue most commonly seen not only in the pediatric population but also in adolescents and adults due to aberrant recreational exposure. As a vulnerable body system, the eyes can also be negatively impacted by hand sanitizer misuse leading to chemical injury, visual impairment, and even blindness. In this review, we aim to highlight the variations in hand sanitizer formulation, the benefits, and how misuse or overuse may lead to adverse effects on the skin, gut, and eyes. In particular, we review the advantages and disadvantages of alcohol-based hand sanitizers (ABHSs) and non-alcohol-based hand sanitizers (NABHSs) and how the components and chemicals used in each can contribute to organ dysbiosis and systemic damage.

The health of bees can be assessed through their microbiome, which serves as a biomarker indicating the presence of both beneficial and harmful microorganisms within a bee community. This study presents the characterisation of the bacterial, fungal, and plant composition on the cuticle of adult bicoloured sweat bees (Agapostemon virescens). These bees were collected using various methods such as pan traps, blue vane traps and sweep netting across the northern extent of their habitat range. Non-destructive methods were employed to extract DNA from the whole pinned specimens of these wild bees. Metabarcoding of the 16S rRNA, ITS and rbcL regions was then performed. The study found that the method of collection influenced the detection of certain microbial and plant taxa. Among the collection methods, sweep net samples showed the lowest fungal alpha diversity. However, minor differences in bacterial or fungal beta diversity suggest that no single method is significantly superior to others. Therefore, a combination of techniques can cater to a broader spectrum of microbial detection. The study also revealed regional variations in bacterial, fungal and plant diversity. The core microbiome of A. virescens comprises two bacteria, three fungi and a plant association, all of which are commonly detected in other wild bees. These core microbes remained consistent across different collection methods and locations. Further extensive studies of wild bee microbiomes across various species and landscapes will help uncover crucial relationships between pollinator health and their environment.

Bacteria of the family Enterobacteriaceae are associated with gastrointestinal (GI) bleeding and bacteremia and are a leading cause of death, from sepsis, for individuals with inflammatory bowel diseases. The bacterial behaviors and mechanisms underlying why these bacteria are prone to bloodstream entry remain poorly understood. Herein, we report that clinical isolates of non-typhoidal Salmonella enterica serovars, Escherichia coli, and Citrobacter koseri are rapidly attracted toward sources of human serum. To simulate GI bleeding, we utilized an injection-based microfluidics device and found that femtoliter volumes of human serum are sufficient to induce bacterial attraction to the serum source. This response is orchestrated through chemotaxis and the chemoattractant L-serine, an amino acid abundant in serum that is recognized through direct binding by the chemoreceptor Tsr. We report the first crystal structures of Salmonella Typhimurium Tsr in complex with L-serine and identify a conserved amino acid recognition motif for L-serine shared among Tsr orthologues. We find Tsr to be widely conserved among Enterobacteriaceae and numerous World Health Organization priority pathogens associated with bloodstream infections. Lastly, we find that Enterobacteriaceae use human serum as a source of nutrients for growth and that chemotaxis and the chemoreceptor Tsr provide a competitive advantage for migration into enterohemorrhagic lesions. We define this bacterial behavior of taxis toward serum, colonization of hemorrhagic lesions, and the consumption of serum nutrients as 'bacterial vampirism', which may relate to the proclivity of Enterobacteriaceae for bloodstream infections.

The synergic role of vitamin D and the intestinal microbiota in the regulation of the immune system has been thoroughly described in the literature. Vitamin D deficiency and intestinal dysbiosis have shown a pathogenetic role in the development of numerous immune-mediated and allergic diseases. The physiological processes underlying aging and sex have proven to be capable of having a negative influence both on vitamin D values and the biodiversity of the microbiome. This leads to a global increase in levels of systemic inflammatory markers, with potential implications for all immune-mediated diseases and allergic conditions. Our review aims to collect and analyze the relationship between vitamin D and the intestinal microbiome with the immune system and the diseases associated with it, emphasizing the effect mediated by sexual hormones and aging.

All microorganisms like bacteria, viruses and fungi that reside within a host environment are considered a microbiome. The number of bacteria almost equal that of human cells, however, the genome of these bacteria may be almost 100 times larger than the human genome. Every aspect of the physiology and health can be influenced by the microbiome living in various parts of our body. Any imbalance in the microbiome composition or function is seen as dysbiosis. Different types of dysbiosis are seen and the corresponding symptoms depend on the site of microbial imbalance. The contribution of the intestinal and extra-intestinal microbiota to influence systemic activities is through interplay between different axes. Whole body dysbiosis is a complex process involving gut microbiome and non-gut related microbiome. It is still at the stage of infancy and has not yet been fully understood. Dysbiosis can be influenced by genetic factors, lifestyle habits, diet including ultra-processed foods and food additives, as well as medications. Dysbiosis has been associated with many systemic diseases and cannot be diagnosed through standard blood tests or investigations. Microbiota derived metabolites can be analyzed and can be useful in the management of dysbiosis. Whole body dysbiosis can be addressed by altering lifestyle factors, proper diet and microbial modulation. The effect of these interventions in humans depends on the beneficial microbiome alteration mostly based on animal studies with evolving evidence from human studies. There is tremendous potential for the human microbiome in the diagnosis, treatment, and prognosis of diseases, as well as, for the monitoring of health and disease in humans. Whole body system-based approach to the diagnosis of dysbiosis is better than a pure taxonomic approach. Whole body dysbiosis could be a new therapeutic target in the management of various health conditions.

Endometriosis is classically defined as a chronic inflammatory heterogeneous disorder occurring in any part of the body, characterized by estrogen-driven periodic bleeding, proliferation, and fibrosis of ectopic endometrial glands and stroma outside the uterus. Endometriosis can take overwhelmingly serious damage to the structure and function of multi-organ, even impair whole-body systems, resulting in severe dysmenorrhea, chronic pelvic pain, infertility, fatigue and depression in 5-10% women of reproductive age. Precisely because of a huge deficiency of cognition about underlying etiology and complex pathogenesis of the debilitating disease, early diagnosis and treatment modalities with relatively minor side effects become bottlenecks in endometriosis. Thus, endometriosis warrants deeper exploration and expanded investigation in pathogenesis. The gut microbiota plays a significant role in chronic diseases in humans by acting as an important participant and regulator in the metabolism and immunity of the body. Increasingly, studies have shown that the gut microbiota is closely related to inflammation, estrogen metabolism, and immunity resulting in the development and progression of endometriosis. In this review, we discuss the diverse mechanisms of endometriosis closely related to the gut microbiota in order to provide new approaches for deeper exploration and expanded investigation for endometriosis on prevention, early diagnosis and treatment.

Childhood malnutrition is a public health challenge of much interest and concern globally. However, a perturbed gut microbiome (GM) may limit some nutrition interventions' effects among healthy children with undernutrition.

This review aimed to evaluate the effects of GM-targeted nutrition interventions on growth outcomes among children (0-59 mo) using published studies in low- and middle-income countries.

The methods were guided by the Cochrane methodology. The literature search was conducted to include articles published from inception to July 2023 in PubMed, Google Scholar, and Cochrane Databases. We identified and included 35 studies among 11,047 children. The analysis was conducted considering various growth parameters in the qualitative synthesis and weight gain (kg) in the meta-analysis.

In the qualitative synthesis, 55.6% of prebiotics, 66.7% of probiotics, 71.4% of synbiotics, and 28.6% of "microbiome complementary feed" studies had significant effects on growth outcomes. Also, prebiotics had more studies with significant effects among healthy children, whereas probiotics, synbiotics, and "microbiome complementary feeds" had more studies with significant effects among children with undernutrition. Nineteen studies were included in the meta-analyses, of which 7 (36.8%) measured GM outcomes. The meta-analysis showed that prebiotics exhibited heterogeneity but had significant effects on weight in the intervention as compared with the control (mean difference [MD]: 0.14 kg; 95% CI: 0.02, 0.25; I2 = 63%, P = 0.02; 4 studies, n = 932). Probiotics had significant effects on weight in the intervention (MD: 0.15 kg; 95% CI: 0.06, 0.25; I2 = 42%, P = 0.05; 8 studies, n = 2437) as compared to the control. However, synbiotics (MD: 0.26 kg; 95% CI: -0.04, 0.56; I2 = 41%, P = 0.17; 4 studies, n = 1896] and "microbiome complementary feed" (MD: -0.03 kg; 95% CI: -0.18, 0.11; I2 = 0%, P = 0.60; 3 studies, n = 733] had no significant effects on weight in the intervention as compared with control.

Although probiotics and synbiotics may be effective at enhancing growth among children, the selection of interventions should be contingent upon health status.This trial was registered at www.crd.york.ac.uk/prospero/ as CRD42023434109.

Hypertension (HTN) is common among athletes and the most recent epidemiologic data reports that cardiovascular (CV) sudden death is significantly greater in African Americans (AAs). Gut microbial dysbiosis (a poorly diverse stool microbial profile) has been associated with HTN in sedentary people but microbial characteristics of athletes with HTN are unknown. Our purpose was to differentiate microbiome characteristics associated with BP status in AA collegiate athletes. Thirty AA collegiate athletes were stratified by normal BP (systolic BP (SBP) ≤130 mmHg; n = 15) and HTN (SBP ≥130 mmHg; n = 15). 16S rRNA gene sequencing was performed on stool samples to identify microbes at the genus level. We did not observe any significant differences in alpha diversity, but beta diversity was different between groups. Principal coordinate analysis was significantly different (PERMANOVA, p < 0.05, R = 0.235) between groups. Spearman rank correlations showed a significant (p < 0.05) correlation between systolic BP and abundances for Adlercreutzia (R = 0.64), Coprococcus (R = 0.49), Granulicatella (R = 0.63), and Veillonella (R = 0.41). Gut microbial characteristics were associated with differentially abundant microbial genus' and BP status. These results will direct future studies to define the functions of these microbes associated with BP in athletes.

The COVID-19 pandemic continues to cause severe global disruption, resulting in significant excess mortality, overwhelming healthcare systems, and imposing substantial social and economic burdens on nations. While most of the attention and therapeutic efforts have concentrated on the acute phase of the disease, a notable proportion of survivors experience persistent symptoms post-infection clearance. This diverse set of symptoms, loosely categorized as long COVID, presents a potential additional public health crisis. It is estimated that 1 in 5 COVID-19 survivors exhibit clinical manifestations consistent with long COVID. Despite this prevalence, the mechanisms and pathophysiology of long COVID remain poorly understood. Alarmingly, evidence suggests that a significant proportion of cases within this clinical condition develop debilitating or disabling symptoms. Hence, urgent priority should be given to further studies on this condition to equip global public health systems for its management. This review provides an overview of available information on this emerging clinical condition, focusing on the affected individuals' epidemiology, pathophysiological mechanisms, and immunological and inflammatory profiles.

Cardiometabolic diseases are leading causes of mortality in Western countries. Well-established risk factors include host genetics, lifestyle, diet, and the gut microbiome. Moreover, gut bacterial communities and their activities can be altered by bacteriophages (also known simply as phages), bacteria-infecting viruses, making these biological entities key regulators of human cardiometabolic health. The manipulation of bacterial populations by phages enables the possibility of using phages in the treatment of cardiometabolic diseases through phage therapy and fecal viral transplants. First, however, a deeper understanding of the role of the phageome in cardiometabolic diseases is required. In this review, we first introduce the phageome as a component of the gut microbiome and discuss fecal viral transplants and phage therapy in relation to cardiometabolic diseases. We then summarize the current state of phageome research in cardiometabolic diseases and propose how the phageome might indirectly influence cardiometabolic health through gut bacteria and their metabolites.

Dysbiosis of the gut microbiome is frequent in the intensive care unit (ICU), potentially leading to a heightened risk of nosocomial infections. Enhancing the gut microbiome has been proposed as a strategic approach to mitigate potential adverse outcomes. While prior research on select probiotic supplements has not successfully shown to improve gut microbial diversity, fermented foods offer a promising alternative. In this open-label phase I safety and feasibility study, we examined the safety and feasibility of kefir as an initial step towards utilizing fermented foods to mitigate gut dysbiosis in critically ill patients.

We administered kefir in escalating doses (60 mL, followed by 120 mL after 12 h, then 240 mL daily) to 54 critically ill patients with an intact gastrointestinal tract. To evaluate kefir's safety, we monitored for gastrointestinal symptoms. Feasibility was determined by whether patients received a minimum of 75% of their assigned kefir doses. To assess changes in the gut microbiome composition following kefir administration, we collected two stool samples from 13 patients: one within 72 h of admission to the ICU and another at least 72 h after the first stool sample.

After administering kefir, none of the 54 critically ill patients exhibited signs of kefir-related bacteremia. No side effects like bloating, vomiting, or aspiration were noted, except for diarrhea in two patients concurrently on laxatives. Out of the 393 kefir doses prescribed for all participants, 359 (91%) were successfully administered. We were able to collect an initial stool sample from 29 (54%) patients and a follow-up sample from 13 (24%) patients. Analysis of the 26 paired samples revealed no increase in gut microbial α-diversity between the two timepoints. However, there was a significant improvement in the Gut Microbiome Wellness Index (GMWI) by the second timepoint (P = 0.034, one-sided Wilcoxon signed-rank test); this finding supports our hypothesis that kefir administration can improve gut health in critically ill patients. Additionally, the known microbial species in kefir were found to exhibit varying levels of engraftment in patients' guts.

Providing kefir to critically ill individuals is safe and feasible. Our findings warrant a larger evaluation of kefir's safety, tolerability, and impact on gut microbiome dysbiosis in patients admitted to the ICU.

NCT05416814; trial registered on June 13, 2022.

Olive oil, essential ingredient of the Mediterranean diet, is attracting a growing interest due to increasing evidence on its beneficial effects on human health. This study investigated whether extra virgin olive oil (EVOO) possess prebiotic properties. Twenty different monovarietal EVOO samples from 5 Marche region cultivars (Italy) were studied. The prebiotic activity of EVOOs was assessed monitoring the selective stimulation of gut bacterial species and the short chain fatty acids (SCFAs) production, using an in vitro fermentation system. All EVOOs selectively stimulated Lactobacillus spp., with a stronger activity than that observed in the inulin fermentation (positive control). Also, the bifidobacteria population increased; this bifidogenic stimulation was of EVOOs from Raggia cultivar. SCFAs appeared significantly higher after 24 h in all EVOO fermentations than in the control. Acetic and propionic acids production was particularly stimulated. Overall, most of the investigated EVOOs had a potential prebiotic activity, similar or stronger than inulin.

Bacteria of the family Enterobacteriaceae are associated with gastrointestinal (GI) bleeding and bacteremia and are a leading cause of death, from sepsis, for individuals with inflammatory bowel diseases. The bacterial behaviors and mechanisms underlying why these bacteria are prone to bloodstream entry remains poorly understood. Herein, we report that clinical isolates of non-typhoidal Salmonella enterica serovars, Escherichia coli, and Citrobacter koseri are rapidly attracted toward sources of human serum. To simulate GI bleeding, we utilized a custom injection-based microfluidics device and found that femtoliter volumes of human serum are sufficient to induce the bacterial population to swim toward and aggregate at the serum source. This response is orchestrated through chemotaxis, and a major chemical cue driving chemoattraction is L-serine, an amino acid abundant in serum that is recognized through direct binding by the chemoreceptor Tsr. We report the first crystal structures of Salmonella Typhimurium Tsr in complex with L-serine and identify a conserved amino acid recognition motif for L-serine shared among Tsr orthologues. By mapping the phylogenetic distribution of this chemoreceptor we found Tsr to be widely conserved among Enterobacteriaceae and numerous World Health Organization priority pathogens associated with bloodstream infections. Lastly, we find that Enterobacteriaceae use human serum as a source of nutrients for growth and that chemotaxis and the chemoreceptor Tsr provides a competitive advantage for migration into enterohaemorrhagic lesions. We term this bacterial behavior of taxis toward serum, colonization of hemorrhagic lesions, and the consumption of serum nutrients, as 'bacterial vampirism' which may relate to the proclivity of Enterobacteriaceae for bloodstream infections.

Cerebrospinal fluid (CSF) analysis is underutilized in patients with glioblastoma (GBM), partly due to a lack of studies demonstrating the clinical utility of CSF biomarkers. While some studies show the utility of CSF cell-free DNA analysis, studies analyzing CSF metabolites in patients with glioblastoma are limited. Diffuse gliomas have altered cellular metabolism. For example, mutations in isocitrate dehydrogenase enzymes (e.g., IDH1 and IDH2) are common in diffuse gliomas and lead to increased levels of D-2-hydroxyglutarate in CSF. However, there is a poor understanding of changes CSF metabolites in GBM patients. In this study, we performed targeted metabolomic analysis of CSF from n = 31 patients with GBM and n = 13 individuals with non-neoplastic conditions (controls), by mass spectrometry. Hierarchical clustering and sparse partial least square-discriminant analysis (sPLS-DA) revealed differences in CSF metabolites between GBM and control CSF, including metabolites associated with fatty acid oxidation and the gut microbiome (i.e., carnitine, 2-methylbutyrylcarnitine, shikimate, aminobutanal, uridine, N-acetylputrescine, and farnesyl diphosphate). In addition, we identified differences in CSF metabolites in GBM patients based on the presence/absence of TP53 or PTEN mutations, consistent with the idea that different mutations have different effects on tumor metabolism. In summary, our results increase the understanding of CSF metabolites in patients with diffuse gliomas and highlight several metabolites that could be informative biomarkers in patients with GBM.

Curcumin (CUR) is a natural polyphenolic substance that has been widely used since ancient times for its multiple beneficial functions. However, whether CUR affects the growth performance of broilers by altering gut microbiota and metabolite and the underlying mechanism are largely unknown. This study was conducted to evaluate the effect of dietary CUR supplementation on growth performance, anti-inflammatory function, intestinal morphology and barrier, cecum microbiota, and metabolite profile of broilers. Sixty-one-day-old male broilers were randomly divided into the control group (CON, fed a control diet) and the CUR group (fed a control diet supplemented with 200 mg/kg CUR) after 2 d of adaptation. Results showed that after feeding to 52-d-old, compared with CON broilers, the CUR broilers showed improved feed utilization efficiency and growth performance. Furthermore, the CUR broilers showed an improved intestinal morphology, which was demonstrated by a lower crypt depth in the jejunum. The 16S rRNA gene sequencing and non-targeted metabonomics (LC-MS/MS) analysis results showed that the cecum microbiota ecology and function were significantly improved, and the abundance of beneficial flora and metabolites were increased, while the harmful bacteria and metabolites were significantly decreased. In addition, RT-qPCR results showed that CUR significantly reduced inflammatory responses, promoted the formation of the mucosal barrier and enhanced digestion, absorption, and transport of lipids and glucose-related gene expression in the intestine. These above findings demonstrated that dietary CUR supplementation improved growth performance, intestinal morphology, and anti-inflammatory functions, mainly by manipulating cecum microbiota and microbiota-derived metabolites, which provides a credible explanation for the growth-promoting effect and anti-inflammatory functions of CUR and aids our understanding of the mechanisms underlying.

The microbiome has shown a correlation with the diet and lifestyle of each population in health and disease, the ability to communicate at the cellular level with the host through innate and adaptative immune receptors, and therefore an important role in modulating inflammatory process related to the establishment and progression of cancer. The oral cavity is one of the most important interaction windows between the human body and the environment, allowing the entry of an important number of microorganisms and their passage across the gastrointestinal tract and lungs. In this review, the contribution of the microbiome network to the establishment of systemic diseases like cancer is analyzed through their synergistic interactions and bidirectional crosstalk in the oral-gut-lung axis as well as its communication with the host cells. Moreover, the impact of the characteristic microbiota of each population in the formation of the multiomics molecular metafirm of the oral-gut-lung axis is also analyzed through state-of-the-art sequencing techniques, which allow a global study of the molecular processes involved of the flow of the microbiota environmental signals through cancer-related cells and its relationship with the establishment of the transcription factor network responsible for the control of regulatory processes involved with tumorigenesis.

Inflammatory bowel diseases (IBDs) are complex medical conditions in which the gut microbiota is attacked by the immune system of genetically predisposed subjects when exposed to yet unclear environmental factors. The complexity of this class of diseases makes them suitable to be represented and studied with network science. In this paper, the metagenomic data of control, Crohn's disease, and ulcerative colitis subjects' gut microbiota were investigated by representing this data as correlation networks and co-expression networks. We obtained correlation networks by calculating Pearson's correlation between gene expression across subjects. A percolation-based procedure was used to threshold and binarize the adjacency matrices. In contrast, co-expression networks involved the construction of the bipartite subjects-genes networks and the monopartite genes-genes projection after binarization of the biadjacency matrix. Centrality measures and community detection were used on the so-built networks to mine data complexity and highlight possible biomarkers of the diseases. The main results were about the modules of Bacteroides, which were connected in the control subjects' correlation network, Faecalibacterium prausnitzii, where co-enzyme A became central in IBD correlation networks and Escherichia coli, whose module has different patterns of integration within the whole network in the different diagnoses.

The effect of temperature on ectothermic organisms in the context of climate change has long been considered in isolation (i.e. as a single driver). This is challenged by observations demonstrating that temperature-dependent growth is correlated to further factors. However, little is known how the chronobiological history of an organism reflected in its adaptation to re-occurring cyclic patterns in its environment (e.g. annual range of photoperiods in its habitat) and biotic interactions with its microbiome, contribute to shaping its realized niche. To address this, we conducted a full-factorial microcosm multi-stressor experiment with the marine diatoms Thalassiosira gravida (polar) and Thalassiosira rotula (temperate) across multiple levels of temperature (4°C; 9°C; 13.5°C) and photoperiod (4 h; 16 h; 24 h), both in the presence or absence of their microbiomes. While temperature-dependent growth of the temperate diatom was constrained by short and long photoperiods, the polar diatom coped with a 24 h photoperiod up to its thermal optimum (9°C). The algal microbiomes particularly supported host growth at the margins of their respective fundamental niches except for the combination of the warmest temperature tested at 24 h photoperiod. Overall, this study demonstrates that temperature tolerances may have evolved interactively and that the mutualistic effect of the microbiome can only be determined once the multifactorial abiotic niche is defined.

The gut microbiota has important functions in the regulation of normal body functions. Alterations of the microbiota are being increasingly linked to various disease states. The microbiome has been manipulated via the administration of stool from animals or humans, for more than 1000 years. Currently, fecal microbiota transplantation can be performed via endoscopic administration of fecal matter to the duodenum or colon or via capsules of lyophilized stools. More recently fecal microbial transplantation has been shown to be very effective for recurrent Clostridoides difficile infection (CDI). In addition there is some evidence of efficacy in the metabolic syndrome and its hepatic manifestation, metabolic associated fatty liver disease (MAFLD), irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD). We review the current literature regarding the microbiome and the pathogenesis and treatment of CDI, MAFLD, IBS and IBD.

Aflatoxin B₁ (AFB₁), a potent food-borne hepatocarcinogen, is the most toxic aflatoxin that induces liver injury in humans and animals. Species-specific sensitivities of aflatoxins cannot be fully explained by differences in the metabolism of AFB₁ between animal species. The gut microbiota are critical in inflammatory liver injury, but it remains to reveal the role of gut microbiota in AFB₁-induced liver injury. Here, mice were gavaged with AFB₁ for 28 days. Then, the modulation of gut microbiota, colonic barrier, and liver pyroptosis and inflammation were analyzed. To further verify the direct role of gut microbiota in AFB₁-induced liver injury, mice were treated with antibiotic mixtures (ABXs) to deplete the microbiota, and fecal microbiota transplantation (FMT) was conducted. The treatment of AFB₁ in mice altered gut microbiota composition, such as increasing the relative abundance of Bacteroides, Parabacteroides, and Lactobacillus, inducing colonic barrier dysfunction and promoting liver pyroptosis. In ABX-treated mice, AFB₁ had little effect on the colonic barrier and liver pyroptosis. Notably, after FMT, in which the mice were colonized with gut microbiota from AFB₁-treated mice, colonic barrier dysfunction, and liver pyroptosis and inflammation were obliviously identified. We proposed that the gut microbiota directly participated in AFB₁-induced liver pyroptosis and inflammation. These results provide new insights into the mechanisms of AFB₁ hepatotoxicity and pave a window for new targeted interventions to prevent or reduce AFB₁ hepatotoxicity.

Intestinal microorganisms play a crucial role in shaping the host immunity and maintaining homeostasis. Nevertheless, alterations in gut bacterial composition may occur and these alterations have been linked with the pathogenesis of several diseases. In surgical practice, studies revealed that the microbiome of patients undergoing surgery changes and several post-operative complications seem to be associated with the gut microbiota composition. In this review, we aim to provide an overview of gut microbiota (GM) in surgical disease. We refer to several studies which describe alterations of GM in patients undergoing different types of surgery, we focus on the impacts of peri-operative interventions on GM and the role of GM in development of post-operative complications, such as anastomotic leak. The review aims to enhance comprehension regarding the correlation between GM and surgical procedures based in the current knowledge. However, preoperative and postoperative synthesis of GM needs to be further examined in future studies, so that GM-targeted measures could be assessed and the different surgery complications could be reduced.

COVID-19, an acute respiratory viral infection conveyed by pneumonia caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has affected millions of individuals globally, and is a public health emergency of international concern. Till now, there are no highly effective therapies for this infection without vaccination. As they can evolve quickly and cross the strain level easily, these viruses are causing epidemics or pandemics that are allied with more severe clinical diseases. A new approach is needed to improve immunity to confirm the protection against emerging viral infections. Probiotics can modify gut microbial dysbiosis, improve the host immune system, and stimulate immune signaling, increasing systemic immunity. Several probiotic bacterial therapies have been proven to decrease the period of bacterial or viral infections. Superinduction of inflammation, termed cytokine storm, has been directly linked with pneumonia and severe complications of viral respiratory infections. In this case, probiotics as potential immunomodulatory agents can be an appropriate candidate to improve the host's response to respiratory viral infections. During this COVID-19 pandemic, any approach that can induce mucosal and systemic immunity could be helpful. Here, we summarize contexts regarding the effectiveness of various probiotics for preventing virus-induced respiratory infectious diseases, especially those that could be employed for COVID-19 patients. In addition, the effects of probiotics, their mechanisms on different aspects of immune responses against respiratory viral infection, and their antiviral properties in clinical findings have been described in detail.

The impact of kimchi intake on weight management has been a topic of interest. We aimed to conduct an epidemiological study to investigate the association between kimchi intake and weight loss. Participants were selected from the Health Examinees cohort study. Kimchi intake was assessed by a 106-item semi-quantitative food frequency questionnaire, including four types of kimchi. Obesity was defined according to the Korean Society for the Study of Obesity guidelines. We performed a correlation analysis among all participants (N = 58 290) and conducted a prospective risk assessment analysis among participants with a baseline BMI value ≥25 kg m^-2 (N = 20 066). In the correlation analysis, higher kimchi consumption was found to be associated with a lower increment in BMI change (men, β 0.169, 95% CI (0.025, 0.313); women, β 0.140, 95% CI (0.046, 0.236)) compared with the lower group. The risk assessment analysis indicated that moderate kimchi consumption is associated with normal weight development in men (Q3, hazard ratio, 1.28, 95% CI (1.06, 1.54)). Baechu [cabbage] kimchi intake also showed a significant association among men participants (all p for trend <0.05). In conclusion, moderate kimchi intake was associated with weight loss among middle-aged and older Koreans, especially in men.

Individuals with celiac disease (CD), non-celiac wheat sensitivity (NCWS), and irritable bowel syndrome (IBS), show overlapping clinical symptoms and experience gut dysbiosis. A limited number of studies so far compared the gut microbiota among these intestinal conditions. This study aimed to investigate the similarities in the gut microbiota among patients with CD, NCWS, and IBS in comparison to healthy controls (HC).

In this prospective study, in total 72 adult subjects, including CD (n = 15), NCWS (n = 12), IBS (n = 30), and HC (n = 15) were recruited. Fecal samples were collected from each individual. A quantitative real-time PCR (qPCR) test using 16S ribosomal RNA was conducted on stool samples to assess the relative abundance of Firmicutes, Bacteroidetes, Bifidobacterium spp., and Lactobacillus spp.

In all groups, Firmicutes and Lactobacillus spp. had the highest and lowest relative abundance respectively. The phylum Firmicutes had a higher relative abundance in CD patients than other groups. On the other hand, the phylum Bacteroidetes had the highest relative abundance among healthy subjects but the lowest in patients with NCWS. The relative abundance of Bifidobacterium spp. was lower in subjects with CD (P = 0.035) and IBS (P = 0.001) compared to the HCs. Also, the alteration of Firmicutes to Bacteroidetes ratio (F/B ratio) was statistically significant in NCWS and CD patients compared to the HCs (P = 0.05).

The principal coordinate analysis (PCoA), as a powerful multivariate analysis, suggested that the investigated gut microbial profile of patients with IBS and NCWS share more similarities to the HCs. In contrast, patients with CD had the most dissimilarity compared to the other groups in the context of the studied gut microbiota.