Ontology highlight
ABSTRACT:
PROVIDER: PRJNA861670 | ENA |
REPOSITORIES: ENA
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Project description:Background and Aims: The impact of cigarette smoke on inflammatory bowel disease has been established by a large number of epidemiological, clinical, and preclinical studies. Exposure to cigarette smoke is associated with a higher risk of developing Crohn’s disease but is inversely correlated with the development, disease risks, progression, and relapse rate of ulcerative colitis. Few mechanistic studies have investigated the effect of cigarette smoke on intestinal inflammation and microbial composition. Methods: Three groups of mice were exposed to three different concentrations of cigarette smoke for a total of 4 weeks, including 5 days of dextran sulfate sodium treatment to induce colitis and a 7-day recovery period. A comprehensive and integrated comparative analysis of the global colon transcriptome and microbiome, as well as classical endpoints, was performed. Results: Cigarette smoke exposure significantly decreased the severity induced colitis. Colon transcriptome analysis revealed that cigarette smoke downregulated specific pathways in a concentration-dependent manner, affecting both the inflammatory state and composition of the gut microbiome. Metagenomics analysis demonstrated that cigarette smoke can modulate dextran sulfate sodium-induced dysbiosis of specific bacterial genera, contributing to resolve the inflammation or accelerate recovery. Conclusions: Cigarette smoke alters gut microbial composition and reduces inflammatory responses in a concentration-dependent manner. The present study lays the foundation for investigating potential molecular mechanisms responsible for the attenuation of colitis by cigarette smoke.
2020-03-03 | E-MTAB-7988 | biostudies-arrayexpress
Project description:Microbial diversity in feces of mice with colitis
| PRJNA669266 | ENA
Project description:Intestinal microbial dysbiosis is associated with Crohn’s disease (CD). However, the mechanisms leading to the chronic mucosal inflammation that characterizes this disease remain unclear. To evaluate causality and mechanisms of disease, we conducted a systems level study of the interactions between the gut microbiota and host in new-onset pediatric patients. We report an altered host proteome in CD patients indicative of impaired mitochondrial functions. A downregulation of mitochondrial proteins implicated in H2S detoxification was observed, while the relative abundance of H2S microbial producers was increased. Network correlation analysis identified Atopobium parvulum as the central hub of H2S producers. Gnotobiotic and conventionalized colitis-susceptible interleukin-10-deficient (Il10-/-) mice demonstrated that A. parvulum induced colitis, a phenotype requiring the presence of the intestinal microbiota. Administration of bismuth, a H2S scavenger, prevented A. parvulum-induced colitis in Il10-/- mice. This study identified host-microbiota interactions that are disturbed in CD patients providing mechanistic insights on CD pathogenesis.
2016-09-29 | PXD002882 | Pride