Effector-host interactome map links type III secretion systems in healthy gut microbiomes to immune modulation.

Does Consuming the Recommend Daily Level of Fiber Prevent Crohn's Disease?

Diagnostic Problems and Advances in Inflammatory Bowel Disease

A Common Barrier Defect for Celiac Disease and Ulcerative Colitis

ABSTRACTMicrobes colonize anatomical sites in health to form commensal microbial communities (e.g., commensal gut microbiota, commensal skin microbiota, commensal oral microbiota). Commensal microbiota has indirect effects on host growth and maturation through interactions with the host immune system. The commensal microbiota was recently introduced as a novel regulator of skeletal growth and morphology at noncraniofacial sites. Further, we and others have shown that commensal gut microbes, such as segmented filamentous bacteria (SFB), contribute to noncraniofacial skeletal growth and maturation. However, commensal microbiota effects on craniofacial skeletal growth and morphology are unclear. To determine the commensal microbiota's role in craniofacial skeletal growth and morphology, we performed craniometric and bone mineral density analyses on skulls from 9‐week‐old female C57BL/6T germ‐free (GF) mice (no microbes), excluded‐flora (EF) specific‐pathogen‐free mice (commensal microbiota), and murine‐pathogen‐free (MPF) specific‐pathogen‐free mice (commensal microbiota with SFB). Investigations comparing EF and GF mice revealed that commensal microbiota impacted the size and shape of the craniofacial skeleton. EF versus GF mice exhibited an elongated gross skull length. Cranial bone length analyses normalized to skull length showed that EF versus GF mice had enhanced frontal bone length and reduced cranial base length. The shortened cranial base in EF mice was attributed to decreased presphenoid, basisphenoid, and basioccipital bone lengths. Investigations comparing MPF mice and EF mice demonstrated that commensal gut microbes played a role in craniofacial skeletal morphology. Cranial bone length analyses normalized to skull length showed that MPF versus EF mice had reduced frontal bone length and increased cranial base length. The elongated cranial base in MPF mice was due to enhanced presphenoid bone length. This work, which introduces the commensal microbiota as a contributor to craniofacial skeletal growth, underscores that noninvasive interventions in the gut microbiome could potentially be employed to modify craniofacial skeletal morphology. © 2023 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.

Ulcerative Colitis and Crohn's Disease Genetics: More Similar Than We Thought?

Manipulation of the Microbiota for Treatment of IBS and IBD—Challenges and Controversies

Genetics and Environmental Interactions Shape the Intestinal Microbiome to Promote Inflammatory Bowel Disease Versus Mucosal Homeostasis

Herpesviruses have been suggested as possible etiological agents of ulcerative colitis and Crohn's disease. Recently, increased numbers of Epstein-Barr virus (EBV)-infected cells have been detected in ulcerative colitis as compared to Crohn's disease. Interestingly, expression levels of the EBV-induced gene 3 (EBI3), a molecule belonging to the interleukin (IL)-12 family, have also been reported to be elevated in ulcerative colitis as compared to Crohn's disease. To test the hypothesis that these observations might be interrelated, ileocolic resection specimens were examined from 16 patients with ulcerative colitis and from 20 patients with Crohn's disease. The presence of EBV-infected cells and of EBI3-expressing cells was determined quantitatively by in situ hybridisation and immunohistochemistry, respectively. Larger number of EBV-infected cells were seen in areas of active inflammation of ulcerative colitis and Crohn's disease as compared to areas of inactive inflammation. However, there was no statistically significant difference between ulcerative colitis and Crohn's disease. Numbers of EBI3-expressing cells were increased in areas of active inflammation of ulcerative colitis and Crohn's disease but again there was no statistically significant difference between the two diseases. Double labelling experiments showed that EBI3 expression occurred only in a small minority of EBV-infected cells in ulcerative colitis and Crohn's disease. These results suggest that increased numbers of EBV-infected cells in areas of active inflammatory bowel disease (IBD) are secondary to influx or local proliferation of inflammatory cells and do not contribute significantly to local production of EBI3. Assessment of the possible role of EBI3 of the pathogenesis of ulcerative colitis or Crohn's disease requires information regarding the expression of other IL-12 family members.

Neither Hide Nor Hair: The Difficulty of Identifying Useful Disease Biomarkers

Monitoring disease activity in inflammatory bowel disease (IBD) is of major importance to prevent long-term complications. Intestinal fatty acid-binding protein (I-FABP) has been identified as a marker for intestinal damage and correlates with the degree of inflammation. The aim of the present study was to evaluate whether I-FABP can predict active disease or remission in Crohn's disease (CD) and ulcerative colitis (UC) in a real-life IBD cohort. In total, 70 patients with endoscopic disease activity available and 194 patients with disease activity on the basis of a stringent combi-score of clinical activity index, C-reactive protein, and fecal calprotectin were included. Plasma I-FABP was compared between patients with active disease and remission. In a small subgroup of CD patients, follow-up samples were analyzed. In CD (139.2 vs. 119.2 pg/ml; P=0.37) and UC (107.8 vs. 151.8 pg/ml; P=0.33), the median I-FABP did not differ in endoscopic active disease versus remission. In UC patients with active disease on the basis of the combi-score, the median I-FABP (106.8 vs. 172.0 pg/ml; P=0.03) was significantly lower than in patients in remission, but not in CD (145.5 vs. 157.5 pg/ml; P=0.29). Neither disease location in CD nor extent of disease in UC influenced I-FABP significantly. I-FABP was not different (P=0.78) in CD patients with a change in disease activity over time. Plasma I-FABP did not differ between endoscopic active disease and remission in both CD and UC. I-FABP was lower in active UC but not CD on the basis of the combi-score. On the basis of these findings, I-FABP has no potential as a novel noninvasive biomarker for disease activity in IBD.

17. Probiotic Lactobacillus abrogates stressor-induced increases in colonic inflammation and shifts to commensal microbe abundance during pathogen challenge

Background Antimicrobial resistance (AMR) in human health associated bacterial pathogens is a serious concern across the globe. Human gastrointestinal tract (GIT) is populated with trillions of microbial species that contribute to nutrient assimilation, host and microbial cell signalling, pathogenesis and antimicrobial resistance (AMR). Indiscriminate usages of antimicrobial in healthcare, livestock, and agriculture provide an evolutionary advantage to the resistant variants. The ascendency of resistant variants threatens the efficacy of most, if not all, of the antimicrobial drugs commonly used to prevent or cure microbial infections. The aim of this current study was to understand the impact of commensal gut microbiota in the emergence of extensively drug-resistant (XDR) enteric pathogens. Methods Commensal anaerobic gut microbiota was isolated from the healthy Indians without a history of hospitalisation and antibiotic intake in last one year. AMR phenotypes were characterised in an anaerobic workstation using commercially avail Epsilometer test (E-test) strip. Genome of all the isolates was sequenced in GS-FLX +pyrosequencer. Genome assembly was done in GS de novo assembler. Genome annotation and analysis of resistance genes were done using Rapid Annotations using Subsystems Technology (RAST) platform. Results AMR traits in enteric bacteria, both in commensals and pathogens, are physically linked with mobile genetic elements (MGEs) and could rapidly disseminate to the bacterial species through horizontal gene transfer (HGT). Among commensal gut microbiota, the highest number of resistance phenotypes (n=12) and AMR encoding functions were detected in Faecalibacterium prausnitzii. Among pathogens, Vibrio cholerae and Klebsiella pneumoniae showed maximum resistance phenotypes (n=22). Genes encoding antibiotic resistance in commensal and pathogenic bacteria are physically linked with MGEs and could disseminate vertically to the progeny and laterally to the distantly related microbial species. Conclusions XDR pathogenic and commensal enteric bacteria are isolated from healthy Indian subjects without a significant history of hospitalisation or antibiotic consumption. Consequently, the transmissible AMR genes present in the genome of gut commensals could be a potential source of resistance functions for the enteric pathogens.

Akkermansia muciniphila in inflammatory bowel disease and colorectal cancer.

Familial occurrence and inheritance studies in inflammatory bowel disease

FMT may increase the proportion of people with active UC who achieve clinical and endoscopic remission. The evidence was very uncertain about whether use of FMT in people with active UC impacted the risk of serious adverse events or improvement in quality of life. The evidence was also very uncertain about the use of FMT for maintenance of remission in people with UC, as well as induction and maintenance of remission in people with CD, and no conclusive statements could be made in this regard. Further studies are needed to address the beneficial effects and safety profile of FMT in adults and children with active UC and CD, as well as its potential to promote longer-term maintenance of remission in UC and CD.