1. Mutual modulation of gut microbiota and the immune system in type 1 diabetes models.
- Author
-
Rosell-Mases E, Santiago A, Corral-Pujol M, Yáñez F, Varela E, Egia-Mendikute L, Arpa B, Cosovanu C, Panosa A, Serrano-Gómez G, Mora C, Verdaguer J, and Manichanh C
- Subjects
- Mice, Animals, Mice, Inbred NOD, B-Lymphocytes, Diabetes Mellitus, Type 1 genetics, Gastrointestinal Microbiome genetics, B-Lymphocyte Subsets
- Abstract
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., (© 2023. The Author(s).)- Published
- 2023
- Full Text
- View/download PDF