Acrylamide Exposure Activates EGFR-PI3K in Intestinal Macrophages to Promote the Onset and Progression of Inflammatory Bowel Disease.

To investigate the impact and mechanisms of acrylamide (AA), an environmental pollutant, on inflammatory bowel disease (IBD). We exposed normal mice and chronic colitis mouse models to AA and examined the pathological changes in intestinal inflammation. Network toxicology was used to analyze the relationship and mechanisms between AA and IBD. The effects of AA on IBD were observed after treatment with EGFR knockout and EGFR inhibitors. AA induced intestinal inflammation in normal mice, presenting symptoms of IBD. Network toxicology analysis revealed that AA is associated with the EGFR-PI3K-mediated inflammatory signaling pathway. AA activates the EGFR-PI3K signaling pathway to promote the progression of IBD, and this effect is inhibited when the EGFR signal is suppressed. AA can induce intestinal inflammation and promote the progression of IBD through the EGFR-PI3K signaling pathway. The EGFR-PI3K signaling pathway is an important therapeutic target for IBD.