结肠炎
拟杆菌
炎症性肠病
失调
炎症
免疫学
胃肠病学
微生物群
粪便
微生物学
疾病
医学
内科学
肠道菌群
生物
细菌
生物信息学
遗传学
作者
Shanieka Staley,Philip Brandon Busbee,Mitzi Nagarkatti,Prakash Nagarkatti
出处
期刊:Journal of Immunology
[American Association of Immunologists]
日期:2023-05-01
卷期号:210 (1_Supplement): 82.19-82.19
被引量:4
标识
DOI:10.4049/jimmunol.210.supp.82.19
摘要
Abstract Colitis is an inflammatory bowel disease characterized by chronic inflammation of the colon with significant disease-associated alterations in the gut microbiome, a term known as microbial dysbiosis. IBDs, are becoming more prevalent in industrialized areas, impacting over 1.6 million Americans. Our lab has previously shown that in mouse models of colitis, Bacteroides acidifaciens (BA) significantly increases in abundance during disease. In fact, disease severity directly correlates with the increase of abundance of this microbe. BA are obligately anaerobic, non-sporing, non-motile, gram-negative rods. This bacterium can degrade protective mucus in the colon and has properties linked to inflammation, such as enhancing immunoglobulin A (IgA) responses and producing short-chain fatty acid (SCFA) acetic acid. This study investigates the effects of the overgrowth of BA in mice with colitis as well as germ-free (GF) mice to access the ability of this microbe to induce or enhance colitis symptoms. Colitis was induced by administering the 3% dextran sulfate sodium (DSS) model. Results showed that compared to disease controls, conventional C57BL/6 mice inoculated with a high dose of BA via oral gavage had more severe colitis symptoms. These mice lost over 20% of their initial body weight, their colons were shorter, and their colons displayed ulcers, redness, and mucosal crystallization, suggesting BA significantly exacerbated the symptoms of DSS-induced colitis. Introducing BA into GF C57BL/6 mice resulted in a colitis-like phenotype with significant reduction in weight-loss and colon lengths. From this data, we deduced that BA may have the potential to induce colitis if overgrowth of this microbe reaches pathogenic levels. Supported by NIH grant (5P20GM103641)
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