Inflammatory monocyte-derived amphiregulin mediates intestinal fibrosis in Crohn’s disease by activating PI3K/AKT

mice exacerbated intestinal fibrosis in DSS-induced colitis mice. These findings reveal that inflammatory monocytes derived-AREG promotes intestinal fibrosis in experimental colitis and CD patients by promoting intestinal fibroblasts activation and proliferation through the PI3K/AKT pathway. Inflammatory monocytes serve as the primary source of AREG in stricturing CD, critically mediating fibroblast-related fibrotic progression in an AREG-dependent manner. Therefore, AREG, the PI3K/AKT pathway and inflammatory monocytes may serve as potential therapeutic targets for intestinal fibrosis in CD.