Interleukin-11 alleviates the pathology in a mouse model of ulcerative colitis

Interaction between fibroblasts and myeloid cells identified as a key process underlying the pathogenesis

The research group led by Dr. Takashi Nishina and Professor Hiroyasu Nakano of the Department of Biochemistry, Toho University Faculty of Medicine, has found that interleukin-11 (IL-11), a protein secreted by fibroblasts during colitis, contributes to the alleviation of the pathology in a mouse model of ulcerative colitis. Furthermore, the researchers have demonstrated that IL-11 production by fibroblasts is regulated by myeloid cells—a type of immune cells. This discovery reveals a novel function of fibroblasts in inflammatory bowel disease and new fibroblast-mediated cell–cell interactions. Colon homeostasis may be maintained by epithelial cells, immune cells, and fibroblasts in the stroma. The findings will facilitate understanding of the pathogenesis of inflammatory bowel disease and homeostatic mechanisms of the colon. The results were published in iScience (electronic version) on January 4, 2023.

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The authors showed that fibroblasts-produced Interleukin (IL)-11, a member of IL-6 family cytokines, ameliorates acute colitis in mouse models. The authors further found that IL-11 production was regulated by reactive oxygen species (ROS) that are produced by myeloid cells. These findings provide that fibroblast-produced IL-11 plays an important role in protecting the mucosal epithelium under acute colitis. Myeloid cell- derived ROS contribute to the attenuation of colitis through the production of IL-11.