IL-1β knockout increases the intestinal abundancy of Akkermansia muciniphila
نویسندگان
چکیده
Abstract The proinflammatory cytokine interleukin-1β (IL-1β) is known to be upregulated in patients suffering from metabolic syndrome. IL-1β contributes insulin resistance obesity and type 2 diabetes, yet its influence on the intestinal microbiome incompletely understood. data presented here demonstrate that mice genetically deficient show a specific alteration of colonisation small group bacteria. Especially Akkermansia muciniphila , bacterium reported inversely associated with obesity, cardiometabolic diseases low-grade inflammation, showed increased knockout mice. In comparative microarray analysis mucus scrapings colon mucosa wildtype mice, angiogenin 4 mRNA was strongly reduced animals. Since presence culture medium significant growth inhibition A. which not detectable for other bacteria tested, induced expression strong candidate responsible suppression colonisation. Thus, indicate might lacking link between inflammation abundance as observed variety chronic inflammatory disorders.
منابع مشابه
The Mucin degrader Akkermansia muciniphila is an abundant resident of the human intestinal tract.
A 16S rRNA-targeted probe, MUC-1437, was designed and validated in order to determine the presence and numbers of cells of Akkermansia muciniphila, a mucin degrader, in the human intestinal tract. As determined by fluorescent in situ hybridization, A. muciniphila accounted more than 1% of the total fecal cells and was shown to be a common bacterial component of the human intestinal tract.
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Fluorescence in situ hybridization and real-time PCR analysis targeting the 16S rRNA gene of Akkermansia muciniphila were performed to determine its presence in the human intestinal tract. These techniques revealed that an A. muciniphila-like bacterium is a common member of the human intestinal tract and that its colonization starts in early life and develops within a year to a level close to t...
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ژورنال
عنوان ژورنال: Beneficial Microbes
سال: 2023
ISSN: ['1876-2883', '1876-2891']
DOI: https://doi.org/10.1163/18762891-20220042