Metagenomic sequencing deepened our knowledge about the role of the intestinal microbiota in human health, and several studies with various methodologies explored its dynamics during antibiotic treatments. We compared the impact of four widely used antibiotics on the gut bacterial diversity. We used plasma and fecal samples collected during and after treatment from healthy volunteers assigned to a 5-day treatment either by ceftriaxone (1 g every 24 h through IV route), ceftazidime/avibactam (2 g/500 mg every 8 h through IV route), piperacillin/tazobactam (1 g/500 mg every 8 h through IV route) or moxifloxacin (400 mg every 24 h through oral route). Antibiotic concentrations were measured in plasma and feces, and bacterial diversity was assessed by the Shannon index from 16S rRNA gene profiling. The relationship between the evolutions of antibiotic fecal exposure and bacterial diversity was modeled using non-linear mixed effects models. We compared the impact of antibiotics on gut microbiota diversity by simulation, using various reconstructed pharmacodynamic indices. Piperacillin/tazobactam was characterized by the highest impact in terms of intensity of perturbation (maximal [IQR] loss of diversity of 27.3% [1.9; 40.0]), while moxifloxacin had the longest duration of perturbation, with a time to return to 95% of baseline value after the last administration of 13.2 d [8.3; 19.1]. Overall, moxifloxacin exhibited the highest global impact, followed by piperacillin/tazobactam, ceftazidime/avibactam and ceftriaxone. Their AUC between day 0 and day 42 of the change of diversity indices from day 0 were, respectively, -13.2 Shannon unit.day [-20.4; -7.9], -10.9 Shannon unit.day [-20.4; -0.6] and -10.1 Shannon unit.day [-18.3; -4.6]. We conclude that antibiotics alter the intestinal diversity to varying degrees, both within and between antibiotics families. Such studies are needed to help antibiotic stewardship in using the antibiotics with the lowest impact on the intestinal microbiota.

Alcohol-associated liver disease (ALD)-encompassing conditions including steatosis, fibrosis, cirrhosis, and hepatocellular carcinoma-refers to hepatic damage arising from excessive or hazardous alcohol consumption, and is now recognized as a significant global health burden. Although the mechanisms underlying ALD remain incompletely understood, several pathways have been substantiated over the last five decades, notably the involvement of intestinal microorganisms and the involvement of the gut-liver axis in alcohol metabolism and ALD pathogenesis. Ethanol intake disrupts the intestinal microbial balance and compromises the gut barrier, resulting in increased permeability to microbial products. The subsequent translocation of microbial metabolites and other antigenic substances to the liver activates hepatic immune responses, thereby contributing to liver injury. In addition, gastrointestinal hormones are also implicated in ALD progression through various mechanisms. Although no therapies for ALD have been approved by the Food and Drug Administration, various therapeutic strategies targeting the intestinal microbiota and gut barrier have been identified. In conclusion, this review discusses the role of the gut-liver axis in alcohol metabolism and ALD pathogenesis and explores the emerging therapeutic strategies.

The interplay among antibiotics, gut microbiota, and disease pathogenesis remains poorly understood, particularly in the context of rare gut bacteria. This study identifies a novel correlation between erythromycin-induced stress and the production of antiangiogenic metabolites in Aneurinibacillus aneurinilyticus, a human gut bacterium. We report the isolation and structural characterization of aneuristatin (1), a metabolite featuring a unique pyrrolo[1,2-a]pyrazine scaffold, along with seven structurally related metabolites (2-8) from A. aneurinilyticus ATCC 12856T. These metabolites were upregulated via the erythromycin-induced activation of the arnA biosynthetic gene. Aneuristatin (1) enhanced prolyl hydroxylase activity, promoting hypoxia-inducible factor-1α (HIF-1α) degradation and reducing downstream targets, including VEGF and EPO. It also exhibited antioxidant effects by reducing ROS levels under hypoxia. Additionally, it inhibited angiogenesis in HUVECs and zebrafish and effectively reduced inflammation, fibrosis, and angiogenesis in a mouse corneal injury model. Our study establishes a molecular basis for the potential of erythromycin-induced aneuristatin (1) to prevent or treat angiogenesis-related diseases such as cancer.

The gut microbiota plays a crucial role in maintaining host health. While numerous studies have explored the impact of antibiotics on the gut microbiota in humans, limited research has examined how antibiotics affect the gut microbiome in dogs. This study investigated the effects of antibiotic treatment on the gut microbiota of dogs and assessed whether probiotic supplementation could prevent antibiotic-induced dysbiosis. Fourteen healthy young dogs undergoing castration were included in the study. All dogs received a single injection of cefovecin immediately after surgery. The probiotics group (7 dogs) was given a probiotic complex daily starting on the day of surgery and continuing for two weeks, while the non-probiotics group (7 dogs) received no supplementation. Fecal samples were collected on the day of surgery and two weeks later during the follow-up visit for suture removal for microbiome analysis. In microbial diversity analysis, α-diversity was significantly higher in the probiotic-supplemented group compared to the non-probiotics group (p < 0.05). β-diversity analysis revealed significant differences in microbial community composition in the non-probiotics group after antibiotic treatment (p < 0.05), while no significant differences were observed in the probiotics group. Relative abundance analysis indicated that Clostridioides, a marker of antibiotic-induced dysbiosis, significantly increased in dogs without probiotics after antibiotic treatment (p < 0.05). In contrast, Butyricicoccus, a butyrate-producing bacterium with gut health benefits, was significantly enriched in the probiotics group (p < 0.05). These findings suggest that probiotic supplementation supports healthier gut microbiome recovery following antibiotic treatment and highlights its potential to enhance gut microbiota restoration and mitigate gut dysbiosis caused by antibiotics.

Recent global burden of disease studies have shown that bacterial infections are responsible for over 13 million deaths worldwide, or 1 in every 8 deaths, each year. Enteric diarrheal infections, in particular, pose a significant challenge and strain on healthcare systems as many are difficult to address pharmaceutically, and thus rely primarily on the patient's own immune system and gut microbiome to fight the infection. Nonetheless, the specific mechanisms behind gut microbiome colonization resistance of enteric pathogens are not well defined and microbiome diversity is difficult to represent and study experimentally. To address this gap, we have constructed an agent-based computational model of the colonic epithelium cross section to investigate the colonic invasion of enteric pathogens. The model focuses on three main regions: epithelial layer, mucosal bilayer, and adjacent lumen, and utilizes four main cell types as agents: anaerobic bacteria, facultative anaerobic bacteria, human goblet cells, and pathogens. Utilizing this model, we are able to describe the healthy microbiome cell localization and dynamics from our mucosal bilayer. In addition, we are also able to investigate the impact of host dietary fiber consumption and simulate pathogen invasion. The model exemplifies the possibility and potential to explore key gut microbiome colonization resistance mechanisms and environmental impacts on the gut microbiome using computational methods.

Immunotherapy combined with chemotherapy has become the first-line treatment for recurrent or metastatic nasopharyngeal carcinoma (RM-NPC). However, the impact of antibiotic (ATB) use on the efficacy of immunotherapy in RM-NPC remains unclear. A total of 200 patients with RM-NPC who started first-line immunotherapy between October 2021 and September 2023 were included. Forty-six patients received ATB within 60 days before and 42 days after the first infusion of immunotherapy (group ATB+), and the remaining 154 patients were in group ATB-. The median progression-free survival (PFS) times of the ATB+ and ATB- groups were 11.20 and 19.87 months, respectively (P = 0.061). The 2-year overall survival (OS) rates of the ATB+ and ATB- groups were 52.6% and 76.7%, respectively (P = 0.001). In multivariate analysis, ATB use was significantly associated with worse OS (hazard ratio = 2.549, P = 0.002). No significant differences were observed between the 2 groups in terms of grade 3+ treatment-related adverse events. ATB use in RM-NPC may reduce the effectiveness of first-line immunotherapy.

Fusobacterium nucleatum (F. nucleatum) is an anaerobic bacterium known for its association with periodontal disease and oral infections. It has been implicated in the development of gastrointestinal diseases such as inflammatory bowel disease and colorectal cancer. Ulcerative colitis (UC), which is characterized by chronic inflammation of the colon, is a condition of unknown etiology with a rising incidence rate, significantly affecting the quality of life for patients. The increased intestinal permeability during UC may facilitate the adherence or invasion of F. nucleatum into the damaged intestinal barrier, leading to exacerbated inflammation.

This article introduces the concept of the oral-gut axis, reviewing existing literature to analyze the role of F. nucleatum in the pathogenesis of UC and exploring its potential pathogenic mechanisms. It also summarizes the latest advances in treating patients with UC who have F. nucleatum and looks forward to prospective therapeutic strategies and the translational prospects of F. nucleatum within the oral-gut axis.

F. nucleatum may be a key player in the pathogenesis of UC, likely due to its invasiveness during periods of increased intestinal permeability. The paper also discusses innovative approaches for the prevention and management of UC exacerbated by F. nucleatum, paving the way for more effective treatment of UC.

The review offers new insights into the complex relationship between the oral microbiome and intestinal diseases, enhancing our understanding of their dynamic interactions. There is a paucity of literature on therapeutic approaches, indicating a need for further clinical research.

Although the human gut microbiome, and its role in health and disease, have been extensively studied in different populations, a comprehensive assessment of gut microbiome composition has not been performed in vulnerable refugee populations. In this study, we hypothesized that overall nutritional status, as indicated by serum micronutrients concentrations, is an important driver of variations in gut microbiome composition. Therefore, gut-microbiome diversity and associated demographic, health and nutritional factors were assessed in adolescent Afghan refugees (n=206). Blood and faecal samples were collected and analysed for nutrition status markers and 16S rRNA gene amplicon-based community profiling, respectively. Bioinformatics and statistical analysis were performed using SPSS, QIIME and R. Overall, 56 distinct phyla, 117 families and 252 genera were identified in the faecal samples. Bacterial diversity (alpha and beta diversity) and the Firmicutes:Bacteroidetes (F/B) ratio were significantly higher in the 15 to 19 year old age group (cf. the 10-14 age group) but were lower in the underweight and vitamin D deficient groups. Furthermore, LEfSe analysis identified significant differences in the relative abundance of bacterial genera based on age, BMI and micronutrient (vitamins and minerals) status. These results were further scrutinised by correlation analysis which confirmed that age, BMI and micronutrient status show significant correlations with F/B ratio and the relative abundance of specific bacterial taxa. Collectively, our study provides the first indication of how the gut-microbiota profile of adolescent Afghan refugees is associated with a range of nutrition-status factors. These findings can thus provide a basis for translational microbiota research aimed at improving the health of such understudied and vulnerable populations.

Our goal is to understand whether there is an association between Abx exposure-and the inferred downstream damage to the intestinal microbiome-and the key patient outcomes of overall survival and rejection following liver transplant.

We conducted a retrospective cohort study of 462 liver transplant recipients treated at a multistate liver transplant (LTx) service during a 7-year period. The association between antibiotic exposure and outcome was tested across models that addressed antibiotic spectrum, duration, and timing relative to transplant. Cox proportional hazard regression was used to evaluate the relationship between antibiotics with survival and rejection.

The observed 1-year survival in this cohort was 95% (95% CI: 93%, 97%), and 20.8% of patients (96/462) experienced rejection at 1 year. In multivariable analyses, exposure to anaerobe-targeting antibiotics for longer than 14 days pretransplant (p = 0.055) or posttransplant (p = 0.040) was significantly associated with reduced 1-year survival. In multivariable analyses, exposure to any anaerobe-targeting Abx posttransplant was significantly associated with an increased risk of rejection (p = 0.001).

Exposure to anaerobic spectrum antibiotics either before or after LTx was associated with poor outcomes during the first year posttransplant and provides an impetus to further characterize the relationship between antibiotic use, microbiota disruption, and cellular immunity in liver transplantation.

The gut microbiome, a dynamic and integral component of human health, has co-evolved with its host, playing essential roles in metabolism, immunity, and disease prevention. Traditional microbiome studies, primarily focused on microbial composition, have provided limited insights into the functional and mechanistic interactions between microbiota and their host. The advent of multi-omics technologies has transformed microbiome research by integrating genomics, transcriptomics, proteomics, and metabolomics, offering a comprehensive, systems-level understanding of microbial ecology and host-microbiome interactions. These advances have propelled innovations in personalized medicine, enabling more precise diagnostics and targeted therapeutic strategies. This review highlights recent breakthroughs in microbiome research, demonstrating how these approaches have elucidated microbial functions and their implications for health and disease. Additionally, it underscores the necessity of standardizing multi-omics methodologies, conducting large-scale cohort studies, and developing novel platforms for mechanistic studies, which are critical steps toward translating microbiome research into clinical applications and advancing precision medicine.

There is mounting evidence for the involvement of the immune system, neuroinflammation and disturbed gut microbiota, or dysbiosis, in attention-deficit/hyperactivity disorder (ADHD). Gut dysbiosis is strongly implicated in many physical, autoimmune, neurological, and neuropsychiatric conditions, however knowledge of its particular pathogenic role in ADHD is sparse. As such, this narrative review examines and synthesizes the available evidence related to inflammation, dysbiosis, and neural processes in ADHD. Minimal differences in microbiota diversity measures between cases and controls were found, however many relative abundance differences were observed at all classification levels (phylum to strain). Compositional differences of taxa important to key gut-brain axis pathways, in particular Bacteroides species and Faecalibacterium, may contribute to inflammation, brain functioning differences, and symptoms, in ADHD. We have identified one possible model of ADHD etiopathogenesis involving systemic inflammation, an impaired blood-brain barrier, and neural disturbances as downstream consequences of gut dysbiosis. Nevertheless, studies conducted to date have varied degrees of methodological rigour and involve diverse participant characteristics and analytical techniques, highlighting a need for additional research.

Antibiotics are a cornerstone of modern medicine, saving countless lives. However, their widespread use presents two major challenges. First, antibiotic-induced changes in the microbiome can disrupt immune function, increasing the susceptibility to diseases associated with these alterations. Second, prolonged antibiotic use fosters the proliferation of antibiotic resistance genes, leading to the emergence of resistant strains and threatening our ability to control infections. These challenges highlight an urgent global health crisis, necessitating in-depth investigation into the multifaceted effects of antibiotic exposure on microbiome dynamics and human health. In this review, we explore the potential effects of antibiotic exposure on the microbiome and its implications for overall health. Additionally, we examine the role of emerging technologies in addressing these challenges and in shaping future antibiotic development. Our goal is to provide insights that will inform more effective public health strategies and interventions aimed at mitigating the adverse consequences of antibiotic use, restoring microbial balance, and improving overall health outcomes.

The healthy gut microbiome is important in maintaining health and preventing various chronic and metabolic diseases through interactions with the host via different gut-organ axes, such as the gut-brain, gut-liver, gut-immune, and gut-lung axes. The human gut microbiome is relatively stable, yet can be influenced by numerous factors, such as diet, infections, chronic diseases, and medications which may disrupt its composition and function. Therefore, microbial resilience is suggested as one of the key characteristics of a healthy gut microbiome in humans. However, our understanding of its definition and indicators remains unclear due to insufficient experimental data. Here, we review the impact of key drivers including intrinsic and extrinsic factors such as diet and antibiotics on the human gut microbiome. Additionally, we discuss the concept of a resilient gut microbiome and highlight potential biomarkers including diversity indices and some bacterial taxa as recovery-associated bacteria, resistance genes, antimicrobial peptides, and functional flexibility. These biomarkers can facilitate the identification and prediction of healthy and resilient microbiomes, particularly in precision medicine, through diagnostic tools or machine learning approaches especially after antimicrobial medications that may cause stable dysbiosis. Furthermore, we review current nutrition intervention strategies to maximize microbial resilience, the challenges in investigating microbiome resilience, and future directions in this field of research.

The intestinal microbiota influences many host biological processes, including metabolism, intestinal barrier functions, and immune responses in the gut and distant organs. Alterations in its composition have been associated with the development of inflammatory disorders and cardiovascular diseases, including Kawasaki disease (KD). KD is an acute pediatric vasculitis of unknown etiology and the leading cause of acquired heart disease in children in the United States. The presence of gastrointestinal symptoms in the acute phase of KD has been associated with an increased risk of treatment resistance and the development of coronary artery aneurysms. Studies report alterations in fecal bacterial communities of patients with KD, characterized by the blooming of pathogenic bacteria and decreased relative abundance of short-chain fatty acid-producing bacteria. However, causality and functionality cannot be established from these observational patient cohorts of KD. This highlights the need for more advanced and rigorous studies to establish causality and functionality in both experimental models of KD vasculitis and patient cohorts. Here, we review the evidence linking an altered gut microbiota composition to the development of KD, assess the potential mechanisms involved in this process, and discuss the potential therapeutic value of these observations.

The disruptive effect of antibiotics on the composition and function of the human microbiota is well established. However, the hypothesis that probiotics can help restore the antibiotic-disrupted microbiota has been advanced, with little consideration of the strength of evidence supporting it. Some clinical data suggest that probiotics can reduce antibiotic-related side effects, including Clostridioides difficile-associated diarrhoea, but there are no data that causally link these clinical effects to microbiota protection or recovery. Substantial challenges hinder attempts to address this hypothesis, including the absence of consensus on the composition of a 'normal' microbiota, non-standardized and evolving microbiome measurement methods, and substantial inter-individual microbiota variation. In this Review, we explore these complexities. First, we review the known benefits and risks of antibiotics, the effect of antibiotics on the human microbiota, the resilience and adaptability of the microbiota, and how microbiota restoration might be defined and measured. Subsequently, we explore the evidence for the efficacy of probiotics in preventing disruption or aiding microbiota recovery post-antibiotic treatment. Finally, we offer insights into the current state of research and suggest directions for future research.

The primary goal of captive primate management is to ensure optimal health and welfare of the animals in our care. Given that the gut microbiome interacts closely with host metabolism, immunity, and even cognition, it represents a potentially powerful tool for identifying subtle changes in health status across a range of body systems simultaneously. However, thus far, it has not been widely tested or implemented as a monitoring tool. In this study, we used longitudinal microbiome sampling of newly arrived chimpanzees at Chimp Haven to explore the feasibility of using the gut microbiome as a health and welfare biomarker in a sanctuary environment. We also tested the hypothesis that a transition to a new living environment, and integration into new social groupings, would result in temporal changes in chimpanzee gut microbiome composition. The collection of longitudinal microbiome data at Chimp Haven was feasible, and it revealed temporal shifts that were unique to each individual and, in some cases, correlated to other known impacts on health and behavior. We found limited evidence for microbial change over time after arrival at Chimp Haven that was consistent across individuals. In contrast, social group and enclosure, and to a lesser extent, age and sex, were associated with differences in gut microbiome composition. Microbiome composition was also associated with overall health status categories. However, many of the effects we detected were most apparent when using longitudinal data, as opposed to single time point samples. Additionally, we found important effects of technical factors, specifically outdoor temperature and time to collection, on our data. Overall, we demonstrate that the gut microbiome has the potential to be effectively deployed as a tool for health and environmental monitoring in a population of sanctuary chimpanzees, but the design must be carefully considered. We encourage other institutions to apply these approaches and integrate health and physiology data to build on the utility of gut microbiome analysis for ensuring the welfare of captive primates in a range of contexts.

The lack of available treatments in pediatric non-cystic fibrosis (non-CF) bronchiectasis is a major concern, especially in the context of the increasing disease burden due to better detection rates with advanced imaging techniques. Recurrent infections in these patients are the main cause of deterioration, leading to impaired lung function and increasing the risk of morbidity and mortality. Since pediatric non-CF bronchiectasis with early recognition and appropriate treatment can be reversible, optimal management is an issue of growing significance. The use of inhaled antibiotics as a treatment option, although a standard of care for CF patients, has been poorly studied in patients with non-CF bronchiectasis, especially in children. In this review, we present the current data on the potential use of inhaled antibiotics in the treatment of non-CF bronchiectasis and assess their safety and efficacy profile, focusing mainly on children. We conclude that inhaled antibiotics as an adjuvant maintenance treatment option could be tried in a subgroup of patients with frequent exacerbations and recent or chronic Pseudomonas aeruginosa infection as they appear to have beneficial effects on exacerbation rate and bacterial load with minimal safety concerns. However, the level of evidence in children is extremely low; therefore, further research is needed on the validity of this recommendation.

Altered gut microbiota has emerged as a major contributing factor to the etiology of chronic conditions in humans. Antibiotic exposure, historically dating back to the mass production of penicillin in the early 1940s, has been proposed as a primary contributor to the cumulative alteration of microbiota over generations. However, the mechanistic link between the antibiotics-altered microbiota and chronic conditions remains unclear.

In this study, we discovered that variants of the key beneficial gut microbe, Akkermansia muciniphila, were selected upon exposure to penicillin. These variants had mutations in the promoter of a TEM-type β-lactamase gene or pur genes encoding the de novo purine biosynthesis pathway, and they exhibited compromised abilities to mitigate host obesity in a murine model. Notably, variants of A. muciniphila are prevalent in the human microbiome worldwide.

These findings highlight a previously unknown mechanism through which antibiotics influence host health by affecting the beneficial capacities of the key gut microbes. Furthermore, the global prevalence of A. muciniphila variants raises the possibility that these variants contribute to global epidemics of chronic conditions, warranting further investigations in human populations. Video Abstract.

Salmonella Typhimurium is a foodborne pathogen threatening livestock and human health. It is highly resistant to commonly used clinical antibiotics, and it is urgently needed to explore new anti-Salmonella treatment schemes. In this study, first, our in vivo mouse experiments showed that Baitouweng decoction (BTW), a classical Traditional Chinese Medicine (TCM) prescription, had good efficacy against Salmonella Typhimurium infection: mitigating weight loss of mice; lowering the bacterial load of liver, spleen, and colon; reducing the production of serum inflammatory factors (interleukin-1β and tumor necrosis factor-α); and decreasing histological index scores than that in the Salmonella Typhimurium infection group. Furthermore, we explored the potential active components and molecular mechanism of BTW in the treatment of Salmonella Typhimurium infection. A total of 465 compounds of BTW were retrieved from herb website and 227 bioactive compounds were identified, 911 potential BTW-related targets and 1,602 disease targets of Salmonella Typhimurium infection were acquired by ten public analytical databases, among them, 188 genes were overlay targets of BTW-Salmonella Typhimurium; String, Metascape, and Cytoscape plug-in Molecular Complex Detection and ClueGo analysis pointed that BTW exerted an anti-Salmonella effect through a multicomponent, multitarget, and multipathway manner, including 10 hub targets (TNF, AKT CASP3, ALB, EGFR, JUN, MAPK, STAT3, VEGFA, and TP53) and 94 pathways such as cell apoptosis, inflammation, and metabolism. Finally, AutoDock Vina showed that the hub target AKT1 with menispermine and quercetin had good binding energy, which was confirmed by the in vitro cellular thermal shift assay and drug affinity responsive target stability assay. This study laid the foundation for further study of BTW mechanism and for further development of BTW anti-Salmonella.

Inflammatory bowel diseases (IBDs), encompassing Crohn's disease and ulcerative colitis, are complex chronic disorders characterized by an intricate interplay between genetic predisposition, immune dysregulation, gut microbiota alterations, and environmental exposures. This review aims to synthesize recent advances in IBD pathogenesis, exploring key mechanisms and potential avenues for prevention and personalized therapy. A comprehensive literature search was conducted across major bibliographic databases, selecting the most recent and impactful studies on IBD pathogenesis. The review integrates findings from multi-omics analyses, single-cell transcriptomics, and longitudinal cohort studies, focusing on immune regulation, gut microbiota dynamics, and environmental factors influencing disease onset and progression. Immune dysregulation, including macrophage polarization (M1 vs. M2) and Th17 activation, emerges as a cornerstone of IBD pathogenesis. Dysbiosis, as a result of reduced alpha and beta diversity and overgrowth of harmful taxa, is one of the main contributing factors in causing inflammation in IBD. Environmental factors, including air and water pollutants, maternal smoking, and antibiotic exposure during pregnancy and infancy, significantly modulate IBD risk through epigenetic and microbiota-mediated mechanisms. While recent advances have supported the development of new therapeutic strategies, deeply understanding the complex dynamics of IBD pathogenesis remains challenging. Future efforts should aim to reduce the burden of disease with precise, personalized treatments and lower the incidence of IBD through early-life prevention and targeted interventions addressing modifiable risk factors.

The tumor microenvironment has recently been well-studied in various gastrointestinal cancers, including colorectal cancer (CRC). The gut microbiota, a collection of microorganisms in the human gastrointestinal tract, is one of the microenvironments associated with colon carcinogenesis. It has been challenging to elucidate the mechanisms by which gut microbiota contributes to carcinogenesis and cancer progression due to complex interactions with the host, including its metabolites and immune and inflammatory responses. Various studies described the influence of diet on reported changes in the composition and microbiota of gut bacteria and its association with CRC. In recent years, metagenomic techniques such as shotgun sequencing and genome-wide association studies focused on understanding the role of the microbiota and the metabolome on early CRCs and colon carcinogenesis to determine if there are modifiable or intervenable targets for CRC. In this review, we will attempt to provide an overview of gut microbiota related to CRC, with particular attention to the findings of recent studies.

Globalization in the 21st century has posed several challenges. In particular, the spread of multidrug-resistant bacterial strains, especially Gram-negative bacteria, which are prevalent in certain regions of the world, is one of the most critical issues. This raises concerns about the risks associated with the booming tourism industry and migratory flows. In fact, even transient colonization with multidrug-resistant strains can present significant challenges to individual, family, and public health. Understanding the epidemiology and mechanisms of resistance, associated risk factors and prevention policies is therefore essential to ensure that strategies are in place to limit the global spread of high-risk bacterial clones and thereby protect public health.

Antimicrobial treatment disrupts human microbiota. The effects of lascufloxacin (LSFX), a new fluoroquinolone, on human microbiota remains unknown. Therefore, in this study, we aimed to evaluate the effects of LSFX administration on the gut and salivary microbiota of healthy participants and those with pneumonia.

LSFX (75 mg, once a day, orally) was administered to healthy adults (healthy group) and adult patients with pneumonia (pneumonia group), and fecal and saliva samples were collected at five time points (Days 0, 3, 7, 14, and 28). Using the collected samples, α- and β-diversity indices, as well as bacterial composition of the gut microbiota and salivary microbiota were analyzed using next-generation sequencing.

In the healthy group, α-diversity indices of the gut and salivary microbiota were reduced and the lowest values on Day 3. For the gut microbiota, the Chao1 index (richness) recovered on Day 28, whereas the Shannon index (evenness) did not. In the salivary microbiota, the Chao1 and Shannon indices did not recover within the 28 day period. The β-diversity indices changed after LSFX administration and subsequently recovered on Day 28. After LSFX administration, the abundance of the Lachnospiraceae family decreased in the gut microbiota, and the abundance of Granulicatella, Streptococcus, Prevotella, Absconditabacteriales(SR1), and Saccharimonadales decreased in the salivary microbiota. In the pneumonia group, the α-diversity indices were lowest on Day 14 after LSFX administration.

We elucidated that LSFX administration differentially affected the gut and salivary microbiota; however, the richness and beta diversity recovered within 28 days.

Fecal microbiota filtrate transfer is discussed as a safe alternative to fecal microbiota transfer (FMT) to treat ulcerative colitis. We investigated modulation of viral and bacterial composition during fecal microbiota filtrate transfer followed by FMT in six patients with active ulcerative colitis (where clinical activity improved in three patients after filtrate transfer) and combined 16S ribosomal RNA gene amplicon sequencing with a virome analysis pipeline including fast viral particle enrichment and metagenome mapping to detect frequencies of 45,033 reference bacteriophage genomes. We showed that after antibiotic treatment and during filtrate transfer, the bacterial community typically adopted a stable composition distinct to that before antibiotic treatment, with no change toward a donor community. FMT in contrast typically changed the bacterial community to a community with similarity to donor(s). There were no indications of an establishment of predominant donor viruses during filtrate transfer but a remodeling of the virome. In contrast, the establishment of donor viruses during FMT correlated with the predicted hosts established during such transfer. Our approach warrants further investigation in a randomized trial to evaluate larger therapeutic interventions in a comparable and efficient manner.

This article aims to explore the role of the human gut microbiota (GM) in the pathogenesis of neurological, psychiatric, and neurodevelopmental disorders, highlighting its influence on health and disease, and investigating potential therapeutic strategies targeting GM modulation.

A comprehensive analysis of the gut microbiota's composition and its interaction with the human body, particularly, its role in neurological and psychiatric conditions, is provided. The review discusses factors influencing GM composition, including birth mode, breastfeeding, diet, medications, and geography. Additionally, it examines the GM's functions, such as nutrient absorption, immune regulation, and pathogen defense, alongside its interactions with the nervous system through the gut-brain axis, neurotransmitters, and short-chain fatty acids (SCFAs).

Alterations in the GM are linked to various disorders, including Parkinson's disease, multiple sclerosis, depression, schizophrenia, ADHD, and autism. The GM influences cognitive functions, stress responses, and mood regulation. Antibiotic use disrupts GM diversity, increasing the risk of metabolic disorders, obesity, and allergic diseases. Emerging therapies such as probiotics, prebiotics, and microbiota transplantation show promise in modulating the GM and alleviating symptoms of neurological and psychiatric conditions.

The modulation of the GM represents a promising approach for personalized treatment strategies. Further research is needed to better understand the underlying mechanisms and to develop targeted therapies aimed at restoring GM balance for improved clinical outcomes.

Sepsis is a life-threatening complication caused by an uncontrolled immune response to infection that can lead to multi-organ dysfunction, including liver injury. Recent research has shown the critical role of gut microbiota in sepsis pathogenesis, with the gut-liver axis playing a crucial role in disease progression. Mechanisms such as the disruption of the gut barrier and liver injury pathways mediated by cytokines, chemokines, adhesion molecules, hydrogen sulfide (H2S). and substance P (SP) have been the focus of recent studies. Some potential biomarkers and gut microbiota-targeted therapies have shown promise as emerging tools for predicting and managing sepsis. This review describes the role of the gut-liver axis in sepsis and the potential of microbiota-targeted therapies and biomarker-driven interventions to improve sepsis outcomes.

Inflammatory bowel disease (IBD) is a group of disorders characterized by an inflammation of the gastrointestinal tract (GIT) and represents a major social and economic burden. Despite ongoing research into the etiology and pathophysiology of this multifactorial disease, treatment options remain limited. From this perspective, the gut microbiota has emerged as a potential player in the pathogenesis of IBD, and animal and human studies support this hypothesis. Indeed, the human gut is one of the most complex ecological communities (composed of 1013-1014 microorganisms) that plays a critical role in human health by influencing normal physiology and disease susceptibility through its collective metabolic activities and host interactions. In addition, live probiotic bacteria present in some food products (which transit through the GIT) have been shown to interact with the host immune system and confer several health benefits. The aim of this review is to provide an overview of the link between Faecalibacterium duncaniae and Escherichia coli and IBD, highlighting the main areas of research in this field. An ecological perspective on the gut microbiota may offer new insights for the development of clinical therapies targeting this bacterial community to improve human health.

This review is engaged in determining the capability of plant pollen as a significant source of evidence for the linkage between suspects and crime location in forensic sciences. Research and review articles were collected from Google Scholar, the Web of Science, and PubMed. Articles were searched using specific keywords such as "Forensic Palynology," "Pollen metabarcoding," "Plant forensics," and "Pollen" AND "criminal investigation." Boolean logic was also utilized to narrow the articles to be included in this review article. Through the literature and exploratory research, it has been observed in the current study that with advancements in technology, forensic palynology has found its application in creating an association between the crime scene and suspected individuals to have a link to it, as pollen DNA is a long-lasting investigative tool that can effectively help forensic investigations. Moreover, the literature shows that the DNA of pollen and spores has helped forensic scientists link suspects to crime scenes, and the introduction of pollen DNA metabarcoding tools has eased the efforts of palynologists to analyze pollen DNA. The introduction of DNA metabarcoding techniques to analyze pollen from plants has helped identify the geological locations of the plants and ultimately identify the culprit.

Clostridioides difficile is a toxin-producing bacteria that is a main cause of antibiotic-associated diarrhea. Clostridioides difficile infections (CDI) are associated with disruptions within the gastrointestinal (GI) microbiota which can be further exacerbated by CDI-targeted antibiotic treatment thereby causing recurrent CDI (rCDI) and compounding the burden placed on patients and the healthcare system. Treatment of rCDI consists of antibiotics which can be paired with preventative therapeutics, such as bezlotoxumab or fecal microbiota transplants (FMTs), if sustained clinical response is not obtained. Newer preventative strategies have been recently approved to assist in restoring balance within the GI system with the goal of preventing recurrent infections.

The composition of bacteria in the human colon has been a subject of interest since the beginning of microbiology. With the development of methods for culturing strict anaerobic bacteria under multiple culture conditions, it was shown the gut contained more than 400 bacterial species and different people harbor different abundant species. The term "gut microbiome" in this review refers to bacteria studied in stool samples. Molecular methods for determining the bacterial composition of human gut has revealed more than 3000 species and less than 130 genera, indicating that the diversity of human colonic bacteria is concentrated at the species and strain levels. This review concludes with a discussion of how diversity can lead to unity of individual holobionts, between holobionts, and between populations. One of the reasons for the unity is that different bacterial species can have similar functional genes.

Phage tail-like bacteriocins (tailocins) are protein complexes produced by bacteria with the potential to kill their neighbors. Widespread throughout Gram-negative bacteria, tailocins exhibit extreme specificity in their targets, largely killing closely related strains. Despite their presence in diverse bacteria, the impact of these competitive weapons on the surrounding microbiota is largely unknown. Recent studies revealed the rapid evolution and genetic diversity of tailocins in microbial communities and suggest that there are constraints on the evolution of specificity and resistance. Given the precision of their targeted killing and the ease of engineering new specificities, understanding the evolution and ecological impact of tailocins may enable the design of promising candidates for novel targeted antibiotics.

Although antibiotics remain the mainstay of urinary tract infection treatment, many affected women can be caught in a vicious cycle in which antibiotics given to eradicate one infection predispose them to develop another. This effect is primarily mediated by disturbances in the gut microbiome that both directly enrich for uropathogenic overgrowth and induce systemic alterations in inflammation, tissue permeability, and metabolism that also decrease host resistance to infection recurrences. Here, we discuss nonantibiotic approaches to manipulating the gut microbiome to reverse the systemic consequences of antibiotics, including cranberry supplementation and other dietary approaches, probiotic administration, and fecal microbiota transplantation.

To investigate the relationship between recent antibiotic exposure and the development of coronary artery lesions (CALs) during the clinical course of Kawasaki disease (KD).

Data were obtained from the 25th nationwide epidemiological survey of KD conducted in Japan from 2017 to 2018. Baseline characteristics and clinical course were compared between Antibiotics (+) and Antibiotics (-) groups.

Nationwide survey of KD in Japan.

KD patients were enrolled by response to a questionnaire sent to physicians working in pediatrics at hospitals with >100 beds.

Antibiotic exposure within one week before the first hospital visit as KD patients.

The relationship between recent antibiotic exposure and the development of coronary artery lesions (CALs).

Out of 28,265 KD patients, 12,918 (45.7%) received antibiotics. In KD patients who received antibiotics in the week before KD diagnosis, the frequency of coronary artery lesions (CALs) at each phase were significantly higher compared to those who did not receive antibiotics. In further analysis using propensity score matching, recent antibiotic exposure and the initial IVIG resistance were associated with CALs at the acute and the sequelae phase. After adjusting for the status of initial IVIG resistance, recent antibiotic exposure remained associated with CALs during the acute phase (adjusted OR 1.29, 95%CI 1.16, 1.43) and the sequelae phase (1.26, 95%CI 1.04, 1.52).

These observations suggest that recent antibiotic exposure might be associated with higher frequency of CAL development in KD patients, possibly by altering the gut microbiota and diminishing beneficial bacteria.

Patients with inflammatory bowel disease (IBD) have an increased risk of Clostridioides difficile infection (CDI) compared with those without IBD, which is worsened with antibiotic usage. While prior studies have shown a correlation between CDI development and certain classes of antibiotics, the IBD population has not been well represented. This study evaluates the rates of CDI with outpatient antibiotic use in patients with IBD.

We conducted a retrospective cohort study composed of patients with IBD and compared the incidence of CDI in patients who received an outpatient prescription for antibiotics (6694 patients) against those without prescriptions (6025 patients) from 2014 to 2020 at our institution. We compared CDI rates based on nine antibiotic classes: penicillins, cephalosporins, sulfonamides, tetracyclines, macrolides, quinolones, clindamycin, metronidazole, and nitrofurantoin.

The risk of CDI was low (0.7%) but significantly higher for those with antibiotic exposure (0.9% vs 0.5%, P = 0.005) and had a positive correlation with a smoking history. The increased risk of CDI in the IBD population was attributable to the clindamycin and metronidazole classes (odds ratio = 4.7, 95% confidence interval: 1.9-11.9, P = 0.001; odds ratio = 3.6, 95% confidence interval: 2.1-6.2, P < 0.0001, respectively).

The use of clindamycin or metronidazole prescribed in an outpatient setting was associated with a statistically significant increased risk of CDI in patients with IBD. Although the association between clindamycin and CDI is a well-established and common finding, the association between metronidazole and CDI is unique in this study.

The microbiome-gut-brain axis is altered by environmental stressors such as heat, diet, and pollutants as well as microbes in the air, water, and soil. These stressors might alter the host's microbiome and symbiotic relationship by modifying the microbial composition or location. Compartmentalized mutualistic microbes promote the beneficial interactions in the host leading to circulating metabolites and hormones such as insulin and leptin that affect inter-organ functions. Inflammation and oxidative stress induced by environmental stressors may alter the composition, distribution, and activities of the microbes in the microbiomes such that the resultant metabolite and hormone changes are no longer beneficial. The microbiome-gut-brain axis and immune adverse changes that may accompany environmental stressors are reviewed for effects on innate and adaptive immune cells, which may make host immunity less responsive to pathogens and more reactive to self-antigens. Cardiovascular and fluid exchanges to organs might adversely alter organ functionality. Organs, especially the brain, need a consistent supply of nutrients and clearance of debris; disruption of these exchanges by stressors, and involvement of gut microbiome are discussed regarding neural dysfunctions with Alzheimer's disease, autistic spectrum disorders, viral infections, and autoimmune diseases. The focus of this review includes the manner in which environmental stressors may disrupt gut microbiota leading to adverse immune and hormonal influences on development of neuropathology related to hyperhomocysteinemia, inflammation, and oxidative stress, and how certain therapeutics may be beneficial. Strategies are explored to lessen detrimental effects of environmental stressors on central and peripheral health navigated toward (1) understanding neurological disorders and (2) promoting environmental and public health and well-being.

1. The poultry microbiome and its stability at every point in time, either free range or reared under different farming systems, is affected by several environmental and innate factors. The interaction of the poultry birds with their microbiome, as well as several inherent and extraneous factors contribute to the microbiome dynamics. A poor understanding of this could worsen poultry heath and result in disease/metabolic disorders.2. Many diseased states associated with poultry have been linked to dysbiosis state, where the microbiome experiences some perturbation. Dysbiosis itself is too often downplayed; however, it is considered a disease which could lead to more serious conditions in poultry. The management of interconnected factors by conventional and emerging technologies (sequencing, nanotechnology, robotics, 3D mini-guts) could prove to be indispensable in ensuring poultry health and welfare.3. Findings showed that high-throughput technological advancements enhanced scientific insights into emerging trends surrounding the poultry gut microbiome and ecosystem, the dysbiotic condition, and the dynamic roles of intrinsic and exogenous factors in determining poultry health. Yet, a combination of conventional, -omics based and other techniques further enhance characterisation of key poultry microbiome actors, their mechanisms of action, and roles in maintaining gut homoeostasis and health, in a bid to avert metabolic disorders and infections.4. In conclusion, there is an important interplay of innate, environmental, abiotic and biotic factors impacting on poultry gut microbiome homoeostasis, dysbiosis, and overall health. Associated infections and metabolic disorders can result from the interconnected nature of these factors. Emerging concepts (interkingdom or network signalling and neurotransmitter), and future technologies (mini-gut models, cobots) need to include these interactions to ensure accurate control and outcomes.

Short-chain fatty acids (SCFAs) are the main metabolites produced by bacterial fermentation of dietary fiber within gastrointestinal tract. SCFAs produced by gut microbiotas (GMs) are absorbed by host, reach bloodstream, and are distributed to different organs, thus influencing host physiology. However, due to the limited budget or the poor sensitivity of instruments, most studies on GMs have incomplete blood SCFA data, limiting our understanding of the metabolic processes within the host. To address this gap, we developed an innovative multi-task multi-view integrative approach (M2AE, Multi-task Multi-View Attentive Encoders), to impute blood SCFA levels using gut metagenomic sequencing (MGS) data, while taking into account the intricate interplay among the gut microbiome, dietary features, and host characteristics, as well as the nuanced nature of SCFA dynamics within the body. Here, each view represents a distinct type of data input (i.e., gut microbiome compositions, dietary features, or host characteristics). Our method jointly explores both view-specific representations and cross-view correlations for effective predictions of SCFAs. We applied M2AE to two in-house datasets, which both include MGS and blood SCFAs profiles, host characteristics, and dietary features from 964 subjects and 171 subjects, respectively. Results from both of two datasets demonstrated that M2AE outperforms traditional regression-based and neural-network based approaches in imputing blood SCFAs. Furthermore, a series of gut bacterial species (e.g., Bacteroides thetaiotaomicron and Clostridium asparagiforme), host characteristics (e.g., race, gender), as well as dietary features (e.g., intake of fruits, pickles) were shown to contribute greatly to imputation of blood SCFAs. These findings demonstrated that GMs, dietary features and host characteristics might contribute to the complex biological processes involved in blood SCFA productions. These might pave the way for a deeper and more nuanced comprehension of how these factors impact human health.

Although antibiotics induce sizable perturbations in the human microbiome, we lack a systematic and quantitative method to measure and predict the microbiome's response to specific antibiotics. Here, we introduce such a method, which takes the form of a microbiome response index (MiRIx) for each antibiotic. Antibiotic-specific MiRIx values quantify the overall susceptibility of the microbiota to an antibiotic, based on databases of bacterial phenotypes and published data on intrinsic antibiotic susceptibility. We applied our approach to five published microbiome studies that carried out antibiotic interventions with vancomycin, metronidazole, ciprofloxacin, amoxicillin, and doxycycline. We show how MiRIx can be used in conjunction with existing microbiome analytical approaches to gain a deeper understanding of the microbiome response to antibiotics. Finally, we generate antibiotic response predictions for the oral, skin, and gut microbiome in healthy humans. Our approach is implemented as open-source software and is readily applied to microbiome data sets generated by 16S rRNA marker gene sequencing or shotgun metagenomics.

Antibiotics are potent influencers of the human microbiome and can be a source for enduring dysbiosis and antibiotic resistance in healthcare. Existing microbiome data analysis methods can quantify perturbations of bacterial communities but cannot evaluate whether the differences are aligned with the expected activity of a specific antibiotic. Here, we present a novel method to quantify and predict antibiotic-specific microbiome changes, implemented in a ready-to-use software package. This has the potential to be a critical tool to broaden our understanding of the relationship between the microbiome and antibiotics.

Increasing evidence suggests that alterations in the gut microbiome (GM) play a pivotal role in the pathogenesis of pediatric food allergy (FA). This scoping review analyzes the current evidence on GM features associated with pediatric FAs and highlights the importance of the GM as a potential target of intervention for preventing and treating this common condition in the pediatric age. Following the Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines, we searched PubMed and Embase using the keywords (gut microbiome OR dysbiosis OR gut microbiota OR microbiome signatures) AND (food allergy OR IgE-mediated food allergy OR food protein-induced allergic proctocolitis OR food protein-induced enterocolitis OR non-IgE food allergy OR cow milk allergy OR hen egg allergy OR peanut allergy OR fish allergy OR shellfish allergy OR tree nut allergy OR soy allergy OR wheat allergy OR rice allergy OR food sensitization). We included 34 studies reporting alterations in the GM in children affected by FA compared with healthy controls. The GM in pediatric FAs is characterized by a higher abundance of harmful microorganisms (e.g., Enterobacteriaceae, Clostridium sensu stricto, Ruminococcus gnavus, and Blautia spp.) and lower abundance of beneficial bacteria (e.g., Bifidobacteriaceae, Lactobacillaceae, some Bacteroides species). Moreover, we provide an overview of the mechanisms of action elicited by these bacterial species in regulating immune tolerance and of the main environmental factors that can modulate the composition and function of the GM in early life. Altogether, these data improve our knowledge of the pathogenesis of FA and can open the way to innovative diagnostic, preventive, and therapeutic strategies for managing these conditions.

The impact of antibiotics on the gut microbiota in kidney transplant recipients is not well characterized. In this study, we determine the impact of different subclasses of antibiotics on the gut microbiota in a cohort of 168 kidney transplant recipients.

Gut microbiome profiling was performed on 510 fecal specimens using 16S rRNA gene sequencing of the V4-V5 hypervariable region. We classified fecal specimens by antibiotic exposure into 5 categories: Beta-lactam, Fluoroquinolone (FQ), Beta-lactam & FQ Group, Other Antibiotics, and No Antibiotic (No Abx). Mixed-effects regression models were utilized to identify changes in microbial diversity and in the centered log-ratio (CLR) transformed abundance of genera while adjusting for important covariates.

Antibiotic administration was associated with a significant decrease in the Shannon alpha diversity index, a decreased abundance of 11 taxa including Eubacterium and Ruminococcus, and an increased abundance of 16 taxa including Enterococcus and Staphylococcus. Exposure to Beta-lactam antibiotics was associated with an increased abundance of 10 taxa including Enterococcus and a decreased abundance of 5 taxa including Eubacterium while exposure to FQ antibiotics was associated with an increased abundance of 3 taxa and a decreased abundance of 4 taxa including Ruminococcus.

Beta-lactam antibiotics and FQ antibiotics have a profound impact on the gut microbiota in kidney transplant recipients. Given the link of the gut microbiota to infectious complications, antibiotic associated changes in the microbiota may lead to an increased risk for further infections.