| First Author | Gendo Y | Year | 2019 |
| Journal | Inflamm Intest Dis | Volume | 3 |
| Issue | 3 | Pages | 145-154 |
| PubMed ID | 30820436 | Mgi Jnum | J:303426 |
| Mgi Id | MGI:6512180 | Doi | 10.1159/000495462 |
| Citation | Gendo Y, et al. (2019) Dysbiosis of the Gut Microbiota on the Inflammatory Background due to Lack of Suppressor of Cytokine Signalling-1 in Mice. Inflamm Intest Dis 3(3):145-154 |
| abstractText | Background: Both environmental and genetic factors have been implicated in the induction of autoimmune disease. Therefore, it is important to understand the pathophysiological significance of the gut microbiota and host genetic background that contribute to an autoimmune disease such as inflammatory bowel disease (IBD). We have previously reported that mice deficient for suppressor of cytokine signaling-1 (SOCS1), in which SOCS1 expression was restored in T and B cells on an SOCS1(-/-) background (SOCS1(-/-)Tg mice), developed systemic autoimmune diseases accompanied by spontaneous colitis. Methods: To investigate whether the proinflammatory genetic background affects the gut microbiota, we used SOCS1(-/-)Tg mice as a model of spontaneous chronic colitis. Fecal samples were collected from SOCS1(-/-)Tg mice and SOCS1(+/+)Tg (control) mice at 1 and 6 months of age, and the fecal bacterial 16S ribosomal RNA genes were sequenced using the Illumina MiSeq platform. Results: Gut microbial diversity was significantly reduced and the intestinal bacterial community composition changed in SOCS1(-/-)Tg mice in comparison with the control mice. Interestingly, the population of Prevotella species, which is known to be elevated in ulcerative colitis and colorectal cancer patients, was significantly increased in SOCS1(-/-)Tg mice regardless of age. Conclusion: Taken together, these results suggest that the proinflammatory genetic background owing to SOCS1 deficiency causes dysbiosis of the gut microbiota, which in turn generates a procolitogenic environment. |
