Intestinal Microbiota and Colorectal Cancer in Inflammatory Bowel Disease
Ontology highlight
ABSTRACT:
DISEASE(S): Crohn’s Disease,Inflammatory Bowel Diseases,Intestinal Diseases,Ulcerative Colitis,Colorectal Cancer,Colorectal Neoplasms,Primary Sclerosing Cholangitis,Inflammatory Bowel Disease
PROVIDER: 2211621 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
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Project description:Gut dysbiosis is closely involved in the pathogenesis of inflammatory bowel disease (IBD). However, it remains unclear whether IBD-associated gut dysbiosis plays a primary role in disease manifestation or is merely secondary to intestinal inflammation. Here, we established a humanized gnotobiotic (hGB) mouse system to assess the functional role of gut dysbiosis associated with two types of IBD - Crohn's disease (CD) and ulcerative colitis (UC). In order to explore the functional impact of dysbiotic microbiota in IBD patients on host immune responses, we analyzed gene expression profiles in colonic mucosa of hGB mice colonized with healty (HC), CD, and UC microbiota.
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Project description:Microbial dysbiosis has been identified in adult inflammatory bowel disease (IBD) patients. However, microbial composition and functional interplay between host genetics and microorganisms in early IBD onset remain poorly defined. Here, we identified and demonstrated the causal effect of Atopobium parvulum and the gut microbiota in pediatric IBD. Microbiota and proteomic profiling revealed that the abundance of A. parvulum, a potent H2S producer, was associated with increased disease severity and a concurrent reduction in the expression of the host H2S detoxification pathway. In the Il10-/- mouse model of inflammation, A. parvulum induced severe pancolitis that was dependent on the presence of the gut microbiota. In addition, we demonstrated that administration of bismuth, an H2S scavenger, prevented A. parvulum-induced colitis. Our findings identified Atopobium parvulum as a major mediator of inflammation severity, and revealed an alteration of the balance between the production and detoxification of H2S in the gastrointestinal tract.
2022-02-22 | PXD000690 | Pride
Project description:The human gut is inhabited by a complex ecosystem of microorganisms, encompassing bacteria, viruses, protozoa, and fungi. Recent research has illuminated the significance of the gut fungal microbiota (mycobiota) in shaping host immunity and influencing the onset and progression of various human diseases. While most investigations into gut microbiota have centered on bacteria, accumulating evidence has underscored the role of mycobiota in the development of inflammatory bowel diseases (IBD), including both ulcerative colitis (UC) and Crohn's disease (CD). In this study, we present the isolation of the live Malassezia globosa strains from the intestinal mucosa of UC patients for the first time. We provide a comprehensive analysis of the characteristics and virulence of this fungus. Malassezia, primarily known to inhabit human skin, prompted us to compare the genomes, transcriptomes, and virulence of M. globosa gut isolates with those of M. globosa strains isolated from the skin. This comparative analysis aimed to discern potential niche-specific adaptations of the fungus. Our findings reveal a striking disparity in the pathogenicity of M. globosa isolated from the gut compared to its skin counterpart. In a mouse model, gut-isolated M. globosa exhibited a more pronounced exacerbation of DSS-induced colitis and elevated production of inflammatory cytokines. Additionally, transcriptome analysis indicated that gut isolates of M. globosa display heightened sensitivity to normoxia compared to their skin-isolated counterparts, suggesting adaptation to the hypoxic conditions prevalent in the intestinal mucosal environment
2024-02-01 | GSE254809 | GEO
Project description:Mitochondrial dysfunction is associated with inflammatory bowel diseases (IBD). To understand how microbial-metabolic circuits contribute to intestinal tissue injury, we disrupt mitochondrial function in the intestinal epithelium by deleting heat shock protein 60 (Hsp60Δ/ΔIEC). While metabolic perturbation causes self-resolving tissue injury, regeneration is disrupted in the absence of aryl hydrocarbon receptor (Hsp60Δ/ΔIEC;AhR-/-) or IL-10 (Hsp60Δ/ΔIEC;Il10-/-) leading to IBD-like pathology. Tissue pathology is absent in the distal colon of germfree (GF) Hsp60Δ/ΔIEC mice, highlighting bacterial control of metabolic injury. Selective colonization of GF Hsp60Δ/ΔIEC mice with the synthetic community OMM12 confirms expansion of metabolically-flexible Bacteroides ssp., which generates metabolic injury in mono-colonized mice. Transcriptional profiling of metabolically-impaired epithelium identifies gene signatures, such as Ido1, Nos2, and Duox2, differentiating active from inactive tissue inflammation in 343 tissue sections from Crohn’s disease patients. In conclusion, mitochondrial perturbation of the epithelium causes microbiota-dependent tissue injury and discriminative inflammatory gene profiles with relevance for IBD.
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Project description:Abstract. Background: The cause of ulcerative colitis (UC) is not yet fully understood. Previous research has pointed towards a potential role for mutations in NOD2 in promoting the onset and progression of inflammatory bowel disease (IBD) by altering the microbiota of the gut. However, the relationship between toll-like receptor 4 (TLR4) and gut microbiota in IBD is not well understood. To shed light on this, the interaction between TLR4 and gut microbiota was studied using a mouse model of IBD. Methods: To examine the function of TLR4 signaling in intestinal injury repair, researchers developed Dextran Sulfate Sodium Salt (DSS)-induced colitis and injury models in both wild-type (WT) mice and TLR4 knockout (TLR4-KO) mice. To assess changes in the gut microbiota, 16S rRNA sequencing was conducted on fecal samples from both the TLR4-KO and WT enteritis mouse models. Results: The data obtained depicted a protective function of TLR4 against DSS-induced colitis. The gut microbiota composition was found to vary considerably between the WT and TLR4-KO mice groups as indicated by β-diversity analysis and operational taxonomic units (OTUs) cluster. Statistical analysis of microbial multivariate variables depicted an elevated abundance of Escherichia coli/Shigella, Gammaproteobacteria, Tenerlcutes, Deferribacteres, Enterobacteria, Rikenellaceae, and Proteobacteria in the gut microbiota of TLR4-KO mice, whereas there was a considerable reduction in Bacteroidetes at five different levels of the phylogenetic hierarchy including phylum, class, order, family, and genus in comparison with the WT control. Conclusion: TLR4 may protect intestinal epithelial cells from damage in response to DSS-induced injury by controlling the microbiota in the gut.
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Project description:Chronic inflammation and gut microbiota dysbiosis are risk factors for colorectal cancer. In clinical practice, inflammatory bowel disease (IBD) patients have a greatly increased risk of developing colitis associated colorectal cancer (CAC). However, the basis underlying the initiation of CAC remains to be explored. Systematic filtration through existing genome-wide association study (GWAS) and conditional deletion of Zfp90 in CAC mice model indicated that Zfp90 was a putative oncogene in CAC development. Strikingly, depletion of gut microbiota eliminated the tumorigenic effect of Zfp90 in CAC mice model. Moreover, fecal microbiota transplantation demonstrated Zfp90 promoted CAC depending on gut microbiota. Combining 16s rDNA sequencing in feces specimens from CAC mice model, we speculated that Prevotella copri-defined microbiota might mediate the oncogenic role of Zfp90 in the development of CAC. Mechanistic studies revealed Zfp90 accelerated CAC development through Tlr4-Pi3k-Akt-Nf-κb pathway. Our findings elucidated the crucial role of Zfp90-microbiota-Nf-κb axis in creating a tumor-promoting environment and suggested therapeutic targets for CAC prevention and treatment.
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2022-09-16 | GSE193677 | GEO
Project description:Inflammatory Bowel Disease (IBD) is a progressive disease of the gut and consists of two types, Crohn’s Disease (CD) and Ulcerative Colitis (UC). It is a complex disease involving genetic, microbial, and environmental factors. The incidence of IBD is steadily increasing and current therapeutic options are plateauing. Thus treatments are evolving to 1. deeper levels of remission from clinical to endoscopic and histologic normalization and 2. Embrace novel targets or drug combinations. We explored whole transcriptome data generated in blood specimens sampled from a large cohort of adult IBD and control subjects to provide 1. a granular, objective and sensitive molecular measures of disease activity in the gut and 2. Novel molecular mechanisms and biomarkers underlying IBD pathology.
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Project description:Inflammatory bowel diseases (IBD) are believed to be driven by dysregulated interactions between the host and the gut microbiota. Our goal is to characterize the relationships between mucosal T cells, the host tissue environment and microbial communities in IBD patients to identify new therapeutic targets. We identified 26 predictors from our combined data set that were effective in distinguishing between regions of the intestine undergoing active inflammation and regions that were normal. Network analysis on these 26 predictors revealed SAA1 as the most connected node linking the abundance of the genus Bacteroides with the production of IL17 and IL22 by CD4+ T cells. The SAA1-linked microbial and transcriptome interactions were further validated with data from the pediatric IBD RISK cohort. This study identifies expression of SAA1 as an important link between mucosal T cells, microbial communities and their tissue environment in IBD patients. A combination of FACS, gene expression and microbial profiling can distinguish between intestinal inflammatory states in IBD regardless of disease types.
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