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Gut immune cells control extra-intestinal disease
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Tomohisa Sujino1,
Kentaro Miyamoto2,3,
Takanori Kanai3 |
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1Center for Diagnostic and Therapeutic Endoscopy, Keio University School of Medicine, 2Miyarisan Pham., 3Department of Internal Medicine, Keio University School of Medicine |
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| Inflammatory bowel diseases (IBD) such as ulcerative colitis and Crohn's disease are characterized by chronic inflammation mainly in the intestinal tract, but many of them are known to have extraintestinal complications. We have shown that skin inflammation induced dysbiosis of intestinal bacteria, which in turn induced exacerbation of intestinal inflammation (skin-gut axis), and the signals from intestinal inflammation contributed to the Treg induction via the vagus nerve toward the suppression of intestinal inflammation (brain-gut axis). Recently, it has been shown that disruption of the intestinal microbiota is important not only for IBD but also for brain diseases such as Parkinson's disease. Moreover, multiple sclerosis (MS) has been reported as an extraintestinal complication of IBD in the central nervous system. In the mouse model of multiple sclerosis, Experimental Autoimmune Encephalitis (EAE), T-Helper 17 cells accumulated in the small intestine before the onset of myelitis, and the association between T cells in the small intestine and T cells infiltrating the spinal cord was investigated by single cell RNA-seq and cell tracing techniques revealed that T cells migrated from the intestinal circulation into the spinal cord. We demonstrate how the intestinal homeostasis is involved in the regulation of inflammation not only in the intestinal tract but also in other organs. |
Index Term 1: Immune cells in gut
Index Term 2: Extraintestinal disease
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