| First Author | Rosell-Mases E | Year | 2023 |
| Journal | Nat Commun | Volume | 14 |
| Issue | 1 | Pages | 7770 |
| PubMed ID | 38012160 | Mgi Jnum | J:355295 |
| Mgi Id | MGI:7563452 | Doi | 10.1038/s41467-023-43652-x |
| Citation | Rosell-Mases E, et al. (2023) Mutual modulation of gut microbiota and the immune system in type 1 diabetes models. Nat Commun 14(1):7770 |
| abstractText | The transgenic 116C-NOD mouse strain exhibits a prevalent Th17 phenotype, and reduced type 1 diabetes (T1D) compared to non-obese diabetic (NOD) mice. A cohousing experiment between both models revealed lower T1D incidence in NOD mice cohoused with 116C-NOD, associated with gut microbiota changes, reduced intestinal permeability, shifts in T and B cell subsets, and a transition from Th1 to Th17 responses. Distinct gut bacterial signatures were linked to T1D in each group. Using a RAG-2(-/-) genetic background, we found that T cell alterations promoted segmented filamentous bacteria proliferation in young NOD and 116C-NOD, as well as in immunodeficient NOD.RAG-2(-/-) and 116C-NOD.RAG-2(-/-) mice across all ages. Bifidobacterium colonization depended on lymphocytes and thrived in a non-diabetogenic environment. Additionally, 116C-NOD B cells in 116C-NOD.RAG-2(-/-) mice enriched the gut microbiota in Adlercreutzia and reduced intestinal permeability. Collectively, these results indicate reciprocal modulation between gut microbiota and the immune system in rodent T1D models. |
