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- W4313382004 abstract "Abstract Colitis is an autoimmune disease characterized by acute or chronic inflammation of the large intestine. Currently there is no cure for patients suffering from colitis, and most treatments involve the use of immunosuppressive drugs that can have adverse side-effects or increased toxicity. In the current study, we show that indole-3-carbinol (I3C), a naturally-occurring plant product found in a number of cruciferous vegetables, was able to ameliorates symptoms in two well-established murine colitis models. In particular, I3C was able to prevent weight loss, reverse colon shortening, as well as reduce accumulation of disease-associated infiltrating immune cells and inflammatory biomarkers, such as serum amyloid A. We performed 16S rRNA metagenomic sequencing to investigate alterations in the gut microbiome after induction of colitis by TNBS and treatment with I3C. 16S analysis of cecal flushes and validation by PCR revealed that TNBS-induced colitis leads to a significant increase in the species Bacteroides acidifaciens, whereas colitis mice treated with I3C had decreased levels of this species, comparative to naïve controls. In addition, I3C was able to modulate gut microbial metabolites by way of altering short chain fatty acid (SFCA) production during disease induction. Lastly, transfer of disease and treated fecal material in antibiotic-treated disease mice confirmed I3C-mediated alterations in the gut microbial environment contributed to the ability of this natural compound to alleviate deleterious effects attributed to colitis. Collectively, these data suggest that I3C is able to ameliorate colitis by preventing pathogenic gut microbial dysbiosis and restoring gut microbiome composition to a more homeostatic state." @default.
- W4313382004 created "2023-01-06" @default.
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- W4313382004 date "2017-05-01" @default.
- W4313382004 modified "2023-10-01" @default.
- W4313382004 title "Indole-3-carbinol ameliorates murine colitis symptoms through alterations in gut microbial composition and metabolomic pathways, particularly through decreasing disease-associated Bacteroides acidifaciens species." @default.
- W4313382004 doi "https://doi.org/10.4049/jimmunol.198.supp.218.18" @default.
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