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. 2022 May 6;23(9):5181. doi: 10.3390/ijms23095181

Figure 2.

Figure 2

Role of IMCs upon intestinal inflammatory conditions. (A) Following infection with C. rodentium or S. typhimurium IMCs become activated. By the production of IL-11 and IL-33 pro-fibrogenic cytokines and CCL2 chemokine, they actively support tissue repair and the recruitment of inflammatory monocytes. (B) Fibrosis can be induced by dysregulated wound healing and a number of secreted factors, such as transforming growth factor-β (TGF-β), TL1A, IL-36, and IL-34. These mediators drive the accumulation and differentiation of αSMA+ myofibroblasts which then secrete excess ECM molecules and pro-fibrogenic cytokines. (C) Upon IBD, fibroblasts can be activated by TNF-α of epithelial origin, leading to their increased ICAM-1 expression and fibrogenic potential. Activated T cells can serve as another source of pro-inflammatory cytokines, such as TNF-α, IL-17, and IFN-γ, driving fibroblast activation. As a response, activated fibroblasts secrete pro-inflammatory and pro-fibrogenic cytokines, a vast array of chemokines, upregulate the expression of FAP and podoplanin and interact with macrophages via the OSM-OSMR axis.