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However, the underlying mechanism remains elusive. To investigate the association among retinoic acid-inducible gene-I-like receptors (RLRs) signaling pathway, intestinal bacterial microbiome, microbial tryptophan metabolites, inflammation, and a longer course of T2DM, 14 patients with T2DM and 7 healthy controls were enrolled. 16S rRNA amplicon sequencing and untargeted metabolomics were utilized to analyze the stool samples. RNA sequencing (RNA-seq) was carried out on the peripheral blood samples. Additionally, C57BL\/6J specific pathogen-free (SPF) mice were used. It was found that the longer course of T2DM could lead to a decrease in the abundance of probiotics in the intestinal microbiome. In addition, the production of microbial tryptophan derivative skatole declined as a consequence of the reduced abundance of related intestinal microbes. Furthermore, low abundances of probiotics, such as <jats:italic>Bacteroides<\/jats:italic> and <jats:italic>Faecalibacterium<\/jats:italic>, could trigger the inflammatory response by activating the RLRs signaling pathway. The increased level of the member of TNF receptor-associated factors (TRAF) family, nuclear factor kappa-B (<jats:italic>NF-\u03baB<\/jats:italic>) activator (<jats:italic>TANK<\/jats:italic>), in the animal colon activated nuclear factor kappa B subunit 2 (<jats:italic>NF\u03baB2<\/jats:italic>), resulting in inflammatory damage. In summary, it was revealed that the low abundances of probiotics could activate the RLR signaling pathway, which could in turn activate its downstream signaling pathway, NF-\u03baB, highlighting a relationship among gut microbes, inflammation, and a longer course of T2DM.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Key points<\/jats:title>\n            <jats:p>\n              <jats:list list-type=\"bullet\">\n                <jats:list-item>\n                  <jats:p>\n                    <jats:italic>Hyperglycemia may suppress tryptophanase activity.<\/jats:italic>\n                  <\/jats:p>\n                <\/jats:list-item>\n                <jats:list-item>\n                  <jats:p>\n                    <jats:italic>The low abundance of Bacteroides combined with the decrease of Dopa decarboxylase (DDC) activity may lead to the decrease of the production of tryptophan microbial derivative skatole, and the low abundance of Bacteroides or reduced skatole may further lead to the increase of blood glucose by downregulating the expression of glucagon-like peptide-1 (GLP1).<\/jats:italic>\n                  <\/jats:p>\n                <\/jats:list-item>\n                <jats:list-item>\n                  <jats:p>\n                    <jats:italic>A low abundance of<\/jats:italic> anti-inflammatory bacteria <jats:italic>may induce an inflammatory response by triggering the RLR signaling pathway and then activating its downstream NF-\u03baB signaling pathway in prolonged T2DM.<\/jats:italic>\n                  <\/jats:p>\n                <\/jats:list-item>\n              <\/jats:list>\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1007\/s00253-024-13041-5","type":"journal-article","created":{"date-parts":[[2024,2,15]],"date-time":"2024-02-15T12:02:08Z","timestamp":1707998528000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["A study on the association between gut microbiota, inflammation, and type 2 diabetes"],"prefix":"10.1007","volume":"108","author":[{"given":"Nannan","family":"Liu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuehua","family":"Yan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bohan","family":"Lv","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanxiang","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuehong","family":"Hu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chunyan","family":"Zheng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Siyu","family":"Tao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruxue","family":"Deng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinfang","family":"Dou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Binfang","family":"Zeng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8394-5904","authenticated-orcid":false,"given":"Guangjian","family":"Jiang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,2,15]]},"reference":[{"issue":"1","key":"13041_CR1","doi-asserted-by":"publisher","first-page":"73","DOI":"10.1016\/0006-291x(87)91606-8","volume":"149","author":"JD Adams","year":"1987","unstructured":"Adams JD, Heins MC, Yost GS (1987) 3-Methylindole inhibits lipid peroxidation. 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