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Inulin prebiotic ameliorates type 1 diabetes dictating regulatory T cell homing via CCR4 to pancreatic islets and butyrogenic gut microbiota in murine model

2023; Oxford University Press; Volume: 115; Issue: 3 Linguagem: Inglês

10.1093/jleuko/qiad132

1938-3673

Jhefferson Barbosa Guimarães, Vanessa Fernandes Rodrigues, Ítalo Sousa Pereira, Gabriel Martins da Costa Manso, Jefferson Elias‐Oliveira, Jefferson Antônio Leite, Mariana Camila Gonçalves Miranda, Sarah de Oliveira, Arilson Bernardo dos Santos Pereira Gomes, Ana Maria Caetano Faria, Simone G. Ramos, Vânia Luiza Deperon Bonato, João S. Silva, Marco Aurélio Ramirez Vinolo, Ulliana Marques Sampaio, Maria Teresa Pedrosa Silva Clerici, Daniela Carlos,

Diabetes and associated disorders

Abstract Gut dysbiosis is linked to type 1 diabetes mellitus (T1D). Inulin (INU), a prebiotic, modulates the gut microbiota, promoting beneficial bacteria that produce essential short-chain fatty acids for immune regulation. However, how INU affects T1D remains uncertain. Using a streptozotocin-induced (STZ) mouse model, we studied INU's protective effects. Remarkably, STZ + INU mice resisted T1D, with none developing the disease. They had lower blood glucose, reduced pancreatic inflammation, and normalized serum insulin compared with STZ + SD mice. STZ + INU mice also had enhanced mucus production, abundant Bifidobacterium, Clostridium cluster IV, Akkermansia muciniphila, and increased fecal butyrate. In cecal lymph nodes, we observed fewer CD4+Foxp3+ regulatory T cells expressing CCR4 and more Foxp3+CCR4+ cells in pancreatic islets, with higher CCL17 expression. This phenotype was absent in CCR4-deficient mice on INU. INU supplementation effectively protects against experimental T1D by recruiting CCR4+ regulatory T cells via CCL17 into the pancreas and altering the butyrate-producing microbiota.