The mammalian intestine is a major site of colonization and a starting point of severe infections by Klebsiella pneumoniae. Inflammatory bowel disease (IBD) is an inflammatory disorder of the gut, and host-derived nitrate in IBD confers a luminal growth advantage upon Escherichia coli and Salmonella typhimurium through nitrate respiration in the inflamed gut. However, the impact of nitrate on the growth and pathogenicity of K. pneumoniae in this microenvironment is poorly understood. In this study, we used oral administration of dextran sodium sulphate to induce IBD in mouse models. We then analysed the colonization levels of K. pneumoniae wild-type (WT), the nitrate reductase gene mutant strains (ΔnarG, ΔnarZ and ΔnarGΔnarZ), and the molybdate uptake gene mutant strain (ΔmodA) in the inflamed intestinal tract. Results showed that the growth, intestinal colonization, and extraintestinal dissemination of K. pneumoniae were increased in the intestines of dextran sulphate sodium (DSS)-treated mice. Nitrate in the inflamed bowel conferred a growth advantage to K. pneumoniae through nitrate respiration. The molybdate transport protein ModA regulated nitrate reductase activity to increase the growth, intestinal colonization, and extraintestinal dissemination of K. pneumoniae. Tungstate will be a promising antibacterial agent to tackle K. pneumoniae infections in IBD patients.

Bariatric surgery is highly effective in achieving weight loss in children and adolescents with severe obesity, however the underlying mechanisms are incompletely understood, and gut microbiome changes are unknown. Here, we show that adolescents exhibit significant gut microbiome and metabolome shifts several months after laparoscopic vertical sleeve gastrectomy (VSG), with increased alpha diversity and notably with enrichment of oral-associated taxa. To assess causality of the microbiome/metabolome changes in phenotype, pre-VSG and post-VSG stool was transplanted into germ-free mice. Post-VSG stool was not associated with any beneficial outcomes such as adiposity reduction compared pre-VSG stool. However, post-VSG stool exhibited a potentially inflammatory phenotype with increased intestinal Th17 and decreased regulatory T cells. Concomitantly, we found elevated fecal calprotectin and an enrichment of proinflammatory pathways in a subset of adolescents post-VSG. We show that in some adolescents, microbiome changes post-VSG may have inflammatory potential, which may be of importance considering the increased incidence of inflammatory bowel disease post-VSG.

Partial RAG deficiency (pRD) can manifest with systemic and tissue-specific immune dysregulation, with inflammatory bowel disease (IBD) in 15% of the patients. We aimed at identifying the immunopathological and microbial signatures associated with IBD in patients with pRD and in a mouse model of pRD (Rag1w/w) with spontaneous development of colitis. pRD patients with IBD and Rag1w/w mice showed a systemic and colonic Th1/Th17 inflammatory signature. Restriction of fecal microbial diversity, abundance of pathogenic bacteria, and depletion of microbial species producing short-chain fatty acid were observed, which were associated with impaired induction of lamina propria peripheral Treg cells in Rag1w/w mice. The use of vedolizumab in Rag1w/w mice and of ustekinumab in a pRD patient were ineffective. Antibiotics ameliorated gut inflammation in Rag1w/w mice, but only bone marrow transplantation (BMT) rescued the immunopathological and microbial signatures. Our findings shed new light in the pathophysiology of gut inflammation in pRD and establish a curative role for BMT to resolve the disease phenotype.

Inflammatory bowel disease (IBD) is characterized by recurring gastrointestinal inflammation, accompanied by a significant rise in global prevalence and disease severity. The overaccumulation of reactive oxygen and nitrogen species (RONS) in the intestinal environment disrupts redox homeostasis and drives pathological overgrowth of Escherichia coli, which are central to IBD pathogenesis. Herein, we designed a multifunctional nanozyme (W-PB) to enable sustained and targeted regulation of intestinal homeostasis through dual mechanisms: specific inhibition of E. coli overgrowth during colitis and efficient RONS clearance. To ensure colon-specific delivery, W-PB was encapsulated in an electrostatically crosslinked hydrogel composed of alginate and chitosan. This formulation protects W-PB from degradation in harsh gastrointestinal conditions and releases the nanoparticles selectively under weakly alkaline intestinal pH. The released tungsten ions suppress E. coli growth via competitive displacement of molybdenum in the molybdopterin cofactor, while W-PB simultaneously neutralizes excess RONS to shield intestinal cells from oxidative damage. In DSS-induced colitis models, the W-PB gel demonstrated significant therapeutic efficacy, achieved through intestinal microbiota remodeling and oxidative stress mitigation.

This review and commentary outline the strong rationale for normalizing the abnormal microbiota of patients with ulcerative colitis, Crohn's disease, and pouchitis and focus on strategies to improve current variable outcomes of fecal microbial transplant (FMT) in ulcerative colitis. Applying lessons from successful FMT therapy of recurrent Clostridioides difficile and insights from basic scientific understanding of host/microbial interactions provide strategies to enhance clinical outcomes in IBD. We outline promising approaches to develop novel-defined consortia of live biotherapeutic products and combination treatments to improve current results and to optimize and personalize treatment approaches in individual patients and disease subsets.

The human microbiome is crucial in regulating intestinal and systemic functions. While its role in cardiovascular disease is better understood, the link between intestinal microbiota and valvular heart diseases (VHD) remains largely unexplored.

Peer-reviewed studies on human, animal or cell models analysing gut microbiota profiles published up to April 2024 were included. Eligible studies used 16S rRNA or shotgun sequencing, metabolite profiling by mass spectrometry, and examined osteogenesis or fibrosis signalling in valve cells. Methods and findings were qualitatively analysed, with data charted to summarize study design, materials and outcomes.

Thirteen studies were included in the review: five human, three animal and five in vitro. Of the nine studies on calcific aortic stenosis (CAS), elevated trimethylamine N-oxide (TMAO) levels were linked to an increased risk of cardiovascular events in cohort studies, with CAS patients showing higher levels of Bacteroides plebeius, Enterobacteriaceae, Veillonella dispar and Prevotella copri. In vivo, TMAO promoted aortic valve fibrosis, while tryptophan derivatives stimulated osteogenic differentiation and interleukin-6 secretion in valvular interstitial cells. Two studies on rheumatic mitral valve disease found altered microbiota profiles and lower short-chain fatty acid levels, suggesting potential impacts on immune regulation. Two studies on Barlow's mitral valve disease in animal models revealed elevated TMAO levels in dogs with congestive heart failure, reduced Paraprevotellaceae, increased Actinomycetaceae and dysbiosis involving Turicibacter and E. coli.

TMAO has been mainly identified as a prognostic marker in VHD. Gut microbiota dysbiosis has been observed in various forms of VHD and deserve further study.

Oral bacteria have been found in the colon in pathologies such as inflammatory bowel disease. To ascertain niche coalescence, 2 elements are essential: (i) paired oral/fecal samples and (ii) strain-level resolution. We profiled the microbiota in 283 samples from 39 patients undergoing intensive chemotherapy at baseline (saliva: 49, plaque: 51, stool: 43), week 2 (saliva: 18, plaque: 17, stool: 17), week 3 (saliva: 18, plaque: 21, stool: 21), and week 4 (saliva: 8, plaque: 10, stool: 10) of chemotherapy. Through strain-level analysis of paired samples, we demonstrate strong evidence for a breakdown of niche separation in most patients. The extent of overlap increased with time, particularly in patients with intestinal mucositis. Our findings provide definitive evidence for ectopic colonization of the distal gut by oral bacteria in a disease state, likely facilitated by intestinal mucositis. Microbiota contribution by the mouth to the colon may have consequences for the host.

Microscopic colitis (MC) is a chronic inflammatory disease of the large intestine that primarily affects older adults and presents with chronic diarrhea. The etiology is unknown and there are currently no FDA approved medications or biomarkers for treatment or monitoring of the disease. Emerging evidence have implicated the gut microbiome and metabolome disturbances in MC pathogenesis. We conduct a comprehensive analysis of gut microbial and metabolic changes in a cohort of 683 participants, including 131 patients with active MC, 159 with chronic diarrhea, and 393 age- and sex-matched controls without diarrhea. Stool microbiome and metabolome are profiled using whole-genome shotgun metagenomic sequencing and ultra-high performance liquid chromatography-mass spectrometry, respectively. Compared to controls, eight microbial species including pro-inflammatory oral-typical Veillonella dispar and Haemophilus parainfluenzae, and 11 species, including anti-inflammatory Blautia glucerasea and Bacteroides stercoris are enriched and depleted in MC, respectively. Pro-inflammatory metabolites, including lactosylceramides, ceramides, lysophospholipids, and lysoplasmalogens, are enriched in active MC. Multi-omics analyses reveal robust associations between microbial species, metabolic pathways, and metabolites, suggesting concordant disruptions in MC. Here, we show distinct shifts in gut microbiome and metabolome in MC that can inform the development of non-invasive biomarkers and novel therapeutics.

Periodontal disease (PD), an inflammatory disease initiated by oral microbiota, may aggravate hypertension (HTN). Few studies were employed to characterize the oral microbiota in hypertensive patients with periodontitis. To investigate the interplay between oral microbiota and hypertension in individuals with periodontitis, we initiated a metagenomic sequencing study on subgingival plaque and saliva samples sourced from HTN patients and those with hypertension and periodontitis (PDHTN). Our primary objective was to characterize species serving as pivotal links (bridge species) in exacerbating hypertension induced by periodontal disease. Within subgingival plaque and saliva specimens, we pinpointed 31 and 28 bridge species, respectively. Furthermore, we noted a decrease in the abundance of nitrate-reducing bacteria, such as Actinomyces spp., Rothia spp., and Veillonella spp., in PDHTN samples. Employing network analysis, we distinguished distinct polymicrobial clusters within the two patient groups. These bridge species coalesced into polymicrobial clusters, revealing intricate symbiotic and competitive relationships. To substantiate our findings, we leveraged an angiotensin II-infused animal model of ligature-induced periodontitis (LIP), confirming the contributory role of Filifactor alocis-a selectively analyzed subgingival bridge species-in exacerbating hypertension and upregulating the frequency of renal CD4+IFNγ+ and CD8+IFNγ+ T cells. Our study screened a list of species linking PD and HTN. PD may aggravate HTN by decreasing the abundance of nitrate-reducing bacteria and increasing the abundance of pathogens. Using an animal model, we demonstrated that F. alocis aggravates HTN via the accumulation of IFNγ+ T cells in the kidneys.

Both periodontal disease and hypertension are widely prevalent all over the world. PD may aggravate the development of HTN via oral microbiota. However, few studies were employed to characterize the oral microbiota in hypertensive patients with periodontitis. Here, the present study profiled the oral microbiota in hypertensive participants with periodontitis. We found that the depleted abundance of nitrate-reducing bacteria and the enriched abundance of pathogens. Finally, we validated the role of Filifactor alocis in exacerbating HTN via infiltration of IFNγ+ T cells in mice kidneys. Our study improved the understanding of oral microbiota linking PD and HTN.

Intestinal microbiota and the host's immune system form a symbiotic alliance that sustains normal development and function in the human gut. Changes such as dietary habits among societies in developed countries have led to the development of unbalanced microbial populations in the gut, likely contributing to the dramatic increase in inflammatory diseases in the last few decades. Recent advances in DNA sequencing technologies have tremendously helped to characterize the microbiome associated with disease, both in identifying global alterations and discovering specific biomarkers that potentially contribute to disease pathogenesis, as evidenced by animal studies. Beyond bacterial alterations, non-bacterial components such as fungi, viruses, and microbial metabolites have been implicated in these diseases, influencing immune responses and gut homeostasis. Multi-omics approaches integrating metagenomics, metabolomics, and transcriptomics offer a more comprehensive understanding of the microbiome's role in disease pathogenesis, paving the way for innovative diagnostic and therapeutic strategies. Unraveling the metagenomic profiles associated with disease may facilitate earlier diagnosis and intervention, as well as the development of more personalized and effective therapeutic strategies. This review synthesizes recent and relevant microbiome research studies aimed at characterizing the microbial signatures associated with inflammatory bowel disease, colorectal cancer, and celiac disease.

Cancer metastasis is the leading cause of death in patients. In recent years, there has been a growing recognition of the role of tumor-associated microflora in tumor metastasis. The connection between oral and gut microflora and the tumor microenvironment has also been extensively studied. The migration of oral and gut microflora is closely associated with tumor development. Although there is awareness regarding the significant impact of microbial communities on human health, the focus on their relationship with host organisms, particularly those related to tumor-associated microflora, remains inadequate. As an integral part of the body, the host microflora is crucial for regulating the cancer risk and preventing tumor recurrence. The oral-gut axis plays an indispensable role in human immunity, and many types of cancers, such as colorectal, pancreatic, and breast, are significantly influenced by their internal microbial communities. However, further exploration into the mechanisms underlying the role of the intratumoral microflora in cancer is necessary to achieve a comprehensive understanding. We have summarized and analyzed related articles in PubMed. This article reviews the impact of the oral-gut axis on the human immune system, explores the relationship between the translocation of the oral and intestinal flora and the tumor microenvironment, analyzes the specific mechanisms involved in the translocation of the oral and intestinal microflora during the evolution and progression of tumors, and elaborates on the correlations between the occurrence and development of tumors and the changes in the microflora. Finally, a summary of these abovementioned points is provided.

Although the gut microbiome is associated with cancer development and progression, little is known about the effects of the gut microbiome landscape and the efficacy of immune checkpoint inhibitors (ICI) across cancer types. We investigated the association between the microbiome, clinical features, and ICI efficacy across cancer types in a large nationwide screening project for solid tumors. Among 2,180 patients with advanced solid tumors enrolled in the SCRUM-Japan MONSTAR-SCREEN between October 2019 and September 2021, in the chemotherapy-naïve cohort (n = 817), a high prevalence of oral bacteria was observed in patients using proton pump inhibitors (PPI) and those with upper gastrointestinal cancers, particularly postoperative patients with gastric or pancreatic cancer. Among patients treated with ICIs (n = 333), a high abundance of sequence variants in the gut microbiome was not significantly associated with ICI efficacy across cancer types (HR = 0.94; 95% confidence interval, 0.73-1.21). However, high oral bacteria in feces significantly correlated with a shorter progression-free survival compared with low oral bacteria (median, 4.34 vs. 6.97 months; HR = 1.38; 95% confidence interval, 1.07-1.78). Notably, in patients using PPIs, a higher proportion of oral bacteria influenced progression-free survival outcomes of ICI treatment (median, 3.15 vs. 2.04 months; P = 0.08), unlike in PPI nonusers (median, 7.13 vs. 5.55 months; P = 0.74). This study of the gut microbiome has unveiled significant insights into its landscape and potential impact on ICI efficacy. It highlights that the abundance of oral bacteria in feces may play a critical role in diminishing ICI efficacy among patients using PPIs.

As part of the MONSTAR-SCREEN, a prospective nationwide project for patients with solid tumors, we found that although gut microbiome diversity does not consistently predict ICI efficacy across cancer types, a high level of oral bacteria in the gut is linked to reduced ICI effectiveness, especially in patients using PPIs. These findings highlight the potential clinical impact of microbiome variations on cancer treatment outcomes.

Menopause is characterized by the cessation of menstruation and a decline in reproductive function, which is an intrinsic component of the aging process. However, it has been a frequently overlooked field of women's health. The oral and gut microbiota, constituting the largest ecosystem within the human body, are important for maintaining human health and notably contribute to the healthy aging of menopausal women. Therefore, a comprehensive review elucidating the impact of the gut and oral microbiota on menopause for healthy aging is of paramount importance. This paper presents the current understanding of the microbiome during menopause, with a particular focus on alterations in the oral and gut microbiota. Our study elucidates the complex interplay between the microbiome and sex hormone levels, explores microbial crosstalk dynamics, and investigates the associations between the microbiome and diseases linked to menopause. Additionally, this review explores the potential of microbiome-targeting therapies for managing menopause-related diseases. Given that menopause can last for approximately 30 years, gaining insights into how the microbiome and menopause interact could pave the way for innovative interventions, which may result in symptomatic relief from menopause and an increase in quality of life in women.

Perturbations of the gut microbiota in patients with inflammatory bowel disease (IBD) have been extensively characterised, but changes to the oral microbiome remain understudied. This study aimed to evaluate the oral microbiome of adults with IBD and of matched controls.

Saliva samples and data were obtained from a Canadian population cohort (n = 320). The salivary microbiome was characterised using 16S rRNA gene sequencing and examined for differences between control participants and those with IBD, as well as disease subcategories (Crohn's Disease and Ulcerative Colitis).

Alpha diversity was significantly lower in participants with IBD than controls in unadjusted models and many remained significant after adjusting for covariates. Significant differences in some beta diversity metrics between participants with IBD and controls were found, although these did not remain significant when adjusted for covariates. Ten genera were significantly differentially abundant between cases and controls. Veillonella and Streptococcus were both increased in abundance in IBD cases vs controls (25% vs 22% and 14% vs 12%, respectively).

These results showcase changes in oral microbial diversity and composition in those living with IBD and highlight the potential of using the salivary microbiome as a biomarker for screening or monitoring IBD.

Lead (Pb), a prevalent heavy metal contaminant in aquatic environments, has complex effects on the gut microbiome function of aquatic animals. In this study, metagenomic analysis of Bufo gargarizans tadpoles was carried out following Pb exposure. Moreover, histological analysis was performed on the intestines. The results showed that Pb exposure induced histological damage to the intestinal epithelium. Significant differences in microbial abundance and function were detected in the 200 μg/L Pb group compared to the control group. Specifically, an increase in Bosea and Klebsiella was noted at 200 μg/L Pb, which potentially could induce inflammation in tadpoles. Notably, the decrease in the abundance of glycoside hydrolases subsequent to exposure to 200 μg/L Pb is likely to attenuate carbohydrate metabolism. Furthermore, increased fluoroquinolone-related antibiotic resistance genes (ARGs), phenolic-related ARGs, and iron uptake systems following 200 μg/L Pb exposure might heighten the disease risk for tadpoles. These discoveries augment our comprehension of the influences of Pb on the intestinal well-being of amphibians and offer valuable insights for further assessment of the ecological risks that Pb poses to amphibians.

The human oral microbiome has been associated with multiple inflammatory conditions including inflammatory bowel disease (IBD). Identifying functional changes in oral microbiome by metaproteomics helps understanding the factors driving dysbiosis related to intestinal diseases. However, enriching bacterial cells from oral samples (such as saliva and mouth rinse) rich in host proteins is challenging. Here, we present an Optimized Salivary MetaProteomic sample analysis workflow (OSaMPle) to enrich salivary bacteria and reduce host-derived interferences for in-depth analysis of the oral metaproteome. Compared to a conventional approach, OSaMPle improved the identification of bacterial peptides and proteins by 3.2 folds and 1.7 folds, respectively. Furthermore, applying OSaMPle to analyze mouth rinse samples from IBD patients revealed significant alterations in bacterial protein expressions under disease conditions. Specifically, proteins involved in the fatty acid elongation pathway in Peptostreptococcus were significantly less abundant in IBD patients, whereas proteins associated with the TCA cycle in Neisseria were significantly more abundant. The OSaMPle workflow is capable of processing small-volume oral samples and adaptable to high-throughput automation. It holds promise as a strategy for investigating the functional responses of oral microbiomes under disease conditions and identifying disease-associated microbes with their proteins, providing critical insights for detecting disease-related biomarkers within the oral microbiome.

Hypertension is a prevalent metabolic disorder in the elderly, with its pathogenesis linked to gut microbiota dysbiosis. Recent studies suggested that oral microbiota may also play a role in hypertension development, yet its relationship with hypertension in the elderly remains underexplored.

This cross-sectional study aimed to examine the structure of the oral microbiota and its association with hypertension in elderly patients, providing insights into hypertension prevention and treatment.

A total of 206 subjects (60-89 years) were categorized into normal (CON) and hypertensive (HTN) groups, based on the Chinese Hypertension Guidelines. Saliva samples were analyzed using 16S rRNA gene sequencing.

Oral microbiota composition was significantly influenced by blood pressure. At the phylum level, Synergistetes and Spirochaetes were more significantly abundant in the HTN group, while at the genus level Treponema and Leptothrix was higher, Actinomyces and Capnocytophaga were lower in HTN. Random Forest analysis identified 15 key microbiota as strong discriminators of HTN (AUC 0.74). Blood pressure was negatively correlated with Actinomycetes and positively correlated with Leptothrix. PICRUST2 analysis revealed elevated chlorinated compound degradation in HTN patients.

This study identified distinct oral microbiota in elderly hypertensive patients, highlighting the role of the oral microbiome in hypertension pathogenesis.

Oral diseases affect approximately 3.5 billion people worldwide, disproportionately burdening populations in developing countries. Chronic diarrhea and constipation, as common intestinal disorders, may interact bidirectionally with oral health, though their population-level associations remain unexamined.

We analyzed data from the National Health and Nutrition Examination Surveys (NHANES) 2005-2008, selecting participants based on inclusion criteria. Chronic diarrhea and constipation were defined based on the bowel health questionnaire. Oral health indicators (teeth condition and oral pain frequency) were derived from the oral health questionnaire. Covariates selected by Lasso regression were analyzed through adjusted logistic regression to examine associations between bowel habits and oral health. Restricted cubic splines (RCS), subgroup stratification, and sensitivity analyses were also used.

A total of 7512 participants aged ≥ 20 with complete information were included. Multivariable logistic regression revealed a significant association between chronic constipation and poor teeth condition (OR:1.45, 95% CI: 1.05-2.01, P = 0.029). A U-shaped dose-response relationship was observed between stool frequency and poor teeth condition (nonlinear P-value = 0.002) using RCS analysis, with both abnormally low and high bowel frequencies correlating with increased oral health risks. No significant association was identified between oral pain frequency and abnormal bowel habits after full covariate adjustment. Stratified analyses indicated that daily dietary fiber intake ≥ 25 g was associated with reduced risks of poor teeth condition (chronic diarrhea OR: 0.40, 95% CI: 0.12-0.98; chronic constipation OR: 0.44, 95% CI: 0.13-1.09), whereas higher income (PIR > 3.5) correlated with elevated risks (chronic diarrhea OR: 2.38, 95% CI: 1.35-3.98; chronic constipation OR: 2.18, 95% CI: 1.22-3.70). Sensitivity analyses supported the stability of associations between abnormal bowel habits and poor teeth condition.

Both chronic constipation and diarrhea were associated with higher risk of poor teeth condition. In the general population and subgroup analyses, individuals with stool frequency around 8-10 times per week demonstrated the lowest risk of poor teeth condition. Stratified analysis indicates that dietary fiber intake and PIR might modify the observed relationship between abnormal bowel habits and teeth condition.

It has been reported that periodontitis was a risk factor for metabolic dysfunction-associated steatotic liver disease (MASLD). The aim of this study is to investigate the impact of periodontitis on all-cause and cause-specific mortality of MASLD patients.

We included 11,019 individuals with metabolic dysfunction-associated steatotic liver disease (MASLD) from the National Health and Nutrition Examination Survey. Multivariable Cox proportional hazards models were utilized to analyze the estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause mortality and cause-specific mortality among participants with different periods of periodontitis status. Additionally, we employed restricted cubic splines (RCS) curves to explore the dose-response relationship between clinical attachment level (CAL) and pocket probing depth (PPD) and mortality rates. Finally, a series of sensitivity analyses and stratification analyses were conducted to test the reliability and robustness of the results.

In this study, moderate to severe periodontitis significantly increased the all-cause mortality (HR 1.29, 95% CI 1.08-1.55; P = 0.003) and cardiovascular disease (CVD)-related mortality (HR 1.41, 95% CI 1.10-1.79; P = 0.006) among MASLD participants. However, no significant effects of different periodontal statuses on cancer mortality were observed among MASLD participants.

A nationwide large-sample longitudinal study indicated that MASLD patients with moderate to severe periodontitis experienced significantly higher all-cause and CVD-related mortality rates compared to those with no or mild periodontitis.

Oral administration of probiotics holds promise for alleviating ulcerative colitis (UC), yet their efficacy is inevitably compromised by the hostile gastrointestinal (GI) environment. Here, we devised a strategy by coating β-glucan (GN) prebiotic onto the surface of Lactobacillus plantarum (Lp) probiotic at the single-cell level (Lp@CGN) based on bioorthogonal chemistry in a layer-by-layer manner. This achieved to form a firm, dense, and multifunctional GN-based "armor" with advances of superior protective properties, colon-targeted degradation, and prebiotic benefits. Under the protection of the prebiotic-based "armor", Lp@CGN exhibited a notable 276-fold increase in the survival rate compared to naïve Lp after exposure to whole GI conditions. Upon reaching the colon, the "armor" was metabolized into short-chain fatty acids (SCFAs) by gut microbiota, facilitating the timely release of Lp within colon, thereby achieving a synergistic treatment effect due to sustained SCFAs generation and Lp liberation. As a result, oral administration of Lp@CGN efficiently realized the alleviation of UC in both preventative and therapeutic models through restoring intestinal mucosal barriers, positively regulating inflammatory cytokines, renovating the dysbiosis of gut microbiota, and promoting SCFAs production. In sum, our strategy marks the reconstruction of probiotics with chemical tools, offering useful insights into powering probiotics for disease treatment.

As the adsorption receptor of bacteriophage tail protein, bacterial lipopolysaccharide (LPS) is a main culprit responsible for nonalcoholic fatty liver disease (NAFLD) caused by high-fat diets. However, few studies have focused on how the interaction between intestinal bacteriophages and bacterial LPS affects the development and progression of NAFLD. Herein, we determined that excessive fat intake significantly increases the levels of endogenous LPS, while the administration of beneficial metabolites of the intestinal microbiota (specifically butyrate) alleviated hepatic injury in rats. The beneficial mechanism of butyrate was attributed to the reprogramming of the structure of the intestinal DNA virome (primarily, phageome). Butyrate possesses the potential to augment bacteriophagic microbial diversity, thereby potentially facilitating interactions between intestinal bacteriophages and bacterial LPS (in the case of homologous phage), further improving mitochondrial dysfunction and reactive oxygen species production, which, in turn, lowered HepG2 cell damage. Likewise, fecal phage transplantation further confirmed that intestinal phages from rats that received butyrate could effectively interact with bacterial LPS to reduce liver damage in rats. Taken together, modifying the intestinal phageome is a promising treatment option for high-fat diet-related NAFLD.

Despite the growing number of studies on the role of gut microbiota in treating gastrointestinal tumors, the overall research trends in this field remain inadequately characterized.

A bibliometric analysis was conducted using publications retrieved from the Web of Science Core Collection (up to September 30, 2024). Analytical tools including VOSviewer, CiteSpace, and an online bibliometric platform were employed to evaluate trends and hotspots.

Analysis of 1,421 publications revealed significant geographical disparities in research output, with China and the United States leading contributions. Institutionally, the University of Adelaide, Zhejiang University, and Shanghai Jiao Tong University were prominent contributors. Authorship analysis identified Hannah R. Wardill as the most prolific author, while the International Journal of Molecular Sciences emerged as a leading journal. Rapidly growing frontiers include "proliferation," "inhibition," "immunotherapy," "drug delivery," and "tumorigenesis."

This study provides a comprehensive overview of research trends and highlights emerging directions, aiming to advance scientific and clinical applications of gut microbiota in gastrointestinal tumor therapy.

Several earlier studies have shown that IBD (including its two subtypes, ulcerative colitis (UC) and Crohn's disease (CD)) increases the risk of periodontal disease. This study aimed to evaluate the relevance among periodontitis and IBD subcategories.

This study was conducted based on PRISMA guidelines. The Web of Science, PubMed, Google Scholar, and Scopus databases were searched up to February 2024 using pertinent keywords. Case series, review articles, and animal studies were excluded. The risk of bias in this research was evaluated through the Joanna Briggs Institute (JBI) criteria. The meta-analysis was conducted using R statistical software.

A total of 9134 patients within 13 studies after the screening process were evaluated. Our study has shown that periodontitis is significantly more prevalent among IBD patients (UC and CD). According to prior meta-analyses, PD morbidity was found to be significantly high among CD patients (OR: 4.30; 95% CI: 3.72-4.98; I2 = 0%). Similarly, UC elevated PD risk (OR: 4.55; 95% CI: 3.76-5.50; I2 = 0%). The risk of periodontitis was not significantly different between CD and UC patients (OR: 0.96; 95% CI: 0.65-1.43; I2 = 34%).

UC and CD patients were more likely to develop periodontitis, with low heterogeneity between studies, while the prevalence of periodontitis among UC and CD patients was not meaningfully different.

The higher risk of periodontitis in patients with IBD indicates the necessity of screening for periodontitis. Considering the various oral manifestations and poor quality of life associated with IBD, it is important to be aware of the symptoms of periodontitis.

As humans, we host personal microbiomes intricately connected to our biology and health. Far from being isolated entities, our microbiomes are dynamically shaped by microbial exchange with the surroundings, in lifelong microbiome acquisition and transmission processes. In this Review, we explore recent studies on how our microbiomes are transmitted, beginning at birth and during interactions with other humans and the environment. We also describe the key methodological aspects of transmission inference, based on the uniqueness of the building blocks of the microbiome - single microbial strains. A better understanding of human microbiome transmission will have implications for studies of microbial host regulation, of microbiome-associated diseases, and for effective microbiome-targeting strategies. Besides exchanging strains with other humans, there is also preliminary evidence we acquire microorganisms from animals and food, and thus a complete understanding of microbiome acquisition and transmission can only be attained by adopting a One Health perspective.

Malnutrition, gut inflammation, and antibiotic induced dysbiosis (AID) are omnipresent risk factors for poor clinical outcomes among critically ill patients. We previously showed that commercially available plant-based enteral nutrition (PBEN) preserves a commensal microbiome when compared to commonly used forms of commercially available artificial enteral nutrition (AEN). This study reveals that PBEN is superior to artificial enteral nutrition (AEN) in recovering from antibiotic-induced dysbiosis (AID) in mice and humans. PBEN effectively mitigates anemia, leukopenia, restores naïve lymphocyte populations, and reduces bone marrow myeloid cell expansion. Animals randomized to PBEN also fared better in response to infectious challenges after antibiotics. A pilot clinical study validated these findings, showing increased gut commensals, reduced pathogens, and improved leukocyte balance in critically ill patients receiving PBEN compared to AEN. These results suggest PBEN offers a practical dietary approach to mitigate antibiotic-associated complications and improve clinical outcomes among hospitalized patients requiring supplemental nutrition.

Streptococcus oralis, a commensal oral Streptococcus, is known as an early colonizer of the tooth surface and causes opportunistic infections, such as bacterial endocarditis. However, its pathogenicity remains unclear. This study aimed to investigate the pathogenicity of S. oralis in vivo using a mouse model. To establish S. oralis-colonized mice, germ-free mice were orally infected with S. oralis. After colonization was confirmed, these infected mice were bred, and their offspring were used as S. oralis-colonized mice. S. oralis was detected only in the intestine of these mice, which exhibited soft stools but no significant inflammation in the examined tissues. Interestingly, S. oralis-colonized mice showed higher urination frequency. Bladder tissue analysis in S. oralis-colonized mice revealed atrophy, edema, fibrosis, and epithelial denudation. RNA sequencing analysis of the bladder in S. oralis-colonized mice indicated higher expression of genes related to chronic inflammation and extracellular matrix organization, and lower expression of genes related to anti-oxidative stress. In this study, we revealed that the commensal bacterium S. oralis induces chronic inflammation and fibrosis in the bladder of mice by intestinal colonization. Hence, our findings indicate that S. oralis has the potential to affect distal tissue beyond the oral cavity, potentially possessing a pathogenic factor involved in non-bacterial cystitis. This study highlights the potential impact of S. oralis on the urinary system of mice.

Inflammatory Bowel Disease (IBD) is an autoimmune disease characterized by chronic relapsing inflammation of the intestinal tract. Gut microbiota (GM) and CD4+T cells are important in the development of IBD. A lot of studies have shown that GM and their metabolites like short-chain fatty acids, bile acids and tryptophan can be involved in the differentiation of CD4+T cells through various mechanisms, which in turn regulate the immune homeostasis of the IBD patients. Therefore, regulating CD4+T cells through GM may be a potential therapeutic direction for the treatment of IBD. Many studies have shown that Traditional Chinese Medicine (TCM) formulas and some herbal extracts can affect CD4+T cell differentiation by regulating GM and its metabolites. In this review, we mainly focus on the role of GM and their metabolites in regulating the differentiation of CD4+T cells and their correlation with IBD. We also summarize the current research progress on the regulation of this process by TCM.

Subacute rumen acidosis (SARA) is a common metabolic disorder in ruminants that disrupts the rumen microbiome and animal health, but diagnosis is challenging due to subtle symptoms and invasive testing requirements. This study explores the potential of the buccal (oral) microbiome as a diagnostic indicator for SARA, hypothesizing an interaction with the rumen microbiome.

The study involved 47 dairy goats, including 11 on a control diet and 36 on high-concentrate diets with increasing rumen-degradable starch. Animals were grouped based on dietary exposure and ruminal pH: Control, Low-RDS Tolerance/SARA (LRDST/LRDSS), and High-RDS Tolerance/SARA (HRDST/HRDSS). Transcriptomics of rumen epithelium showed heightened inflammatory pathway gene expression in SARA-susceptible goats compared to controls and tolerant groups. Alpha diversity of ruminal bacteria showed lower Shannon diversity in HRDSS goats compared to HRDST whereas buccal bacteria displayed significantly lower Chao1 diversity in LRDSS goats compared to HRDST. Beta diversity analyses revealed distinct patterns between SARA-affected goats and healthy controls in both ruminal and buccal microbiomes. Prevotellaceae_UCG-003 emerged as a candidate biomarker, with reduced abundance in SARA-susceptible goats in both rumen and buccal samples. Machine learning classifiers achieved high accuracy in distinguishing SARA-susceptible goats using this genus (rumen AUC = 0.807; buccal AUC = 0.779). Source tracking analysis illustrated diminished cross-population of bacteria from the buccal to rumen (2.86% to 0.25%) and vice versa (8.59% to 1.17%), signifying compromised microbial interchange in SARA-affected goats. A microbiota transplant experiment verified SARA microbiota's ability to induce pH decline, escalate inflammation-related gene expression (MAPK10, IL17B, FOSB, SPP1), disrupt microbial transfer, and reduce Prevotellaceae_UCG-003 in recipients.

Our findings highlight SARA's dual impact on ruminal and buccal microbiota, exacerbating epithelial inflammation gene expression. Shifts in the buccal microbiome, specifically reductions in Prevotellaceae_UCG-003, mirror ruminal changes and can be influenced by inter-compartmental bacterial transmission, thereby offering a non-invasive diagnostic approach for SARA.

The microbiome is crucial for many physiological processes, including immunity, metabolism, and reproduction.

This review aims to contribute to a detailed understanding of the microbiome of the genital tract, which can lead to better management of dysbiosis and reproductive disorders.

Data from the four international information databases Medline, Scopus, Embase, and Google Scholar. The search strategy was based on the combination of the following terms: "microbiota," "microbiome," "microfilm," "microflora," "fertility," or "infertility."

The advent of next-generation sequencing-based technologies during the last decade has revealed the presence of microbial communities in nearly every part of the human body, including the reproductive system. Several studies have shown significant differences between the microbiota of the vagina and endometrium, as well as other parts of the upper genital tract.

The human microbiome plays a critical role in determining a person's health state, and the microbiome of the genital tract may impact fertility potential before and after assisted reproductive treatments (ARTs).

To completely understand the role of the microbiome, future research should focus not only on the description of microbiota but also on the interaction between bacteria, the production of biofilms, and the interaction of microorganisms with human cells.

The oral microbiota, second in abundance to the gut, is implicated in chronic systemic diseases, but its specific role in graft-versus-host disease (GVHD) pathogenesis has been unclear. Our study finds that mucositis-induced oral dysbiosis in patients after hematopoietic cell transplantation (HCT) associated with increased chronic GVHD (cGVHD), even in patients receiving posttransplant cyclophosphamide. In murine HCT models, oral dysbiosis caused by bilateral molar ligatures exacerbated cGVHD and increased bacterial load in the oral cavity and gut, with Enterococcaceae significantly increasing in both organs. In this model, the migration of Enterococcaceae to cervical lymph nodes both before and after transplantation activated antigen-presenting cells, thereby promoting the expansion of donor-derived inflammatory T cells. Based on these results, we hypothesize that pathogenic bacteria increase in the oral cavity might not only exacerbate local inflammation but also enhance systemic inflammation throughout the HCT course. Additionally, these bacteria translocated to the gut and formed ectopic colonies, further amplifying systemic inflammation. Furthermore, interventions targeting the oral microbiome mitigated murine cGVHD. Collectively, our findings highlight the importance of oral dysbiosis in cGVHD and suggest that modulation of the oral microbiome during transplantation may be an effective approach for preventing or treating cGVHD.