Blockade of TLRs-triggered macrophage activation by caffeic acid exerted protective effects on experimental ulcerative colitis.

Ulcerative colitis (UC) represents a relapsing and inflammatory bowel disease which is commonly linked with the communications between dysfunction of epithelium and mucosal immune responses. Though caffeic acid (CA) has numerous pharmacological capacities, whether CA demonstrates immunoregulation on the mucosal immune responses remains ill-defined. Herein, the present research demonstrated that CA could dramatically attenuate the mucosal inflammation, as evidenced by improving the disease severity, serum biochemical indexes, mucosal ulcerations, loss of epithelium and crypts, and secretion of inflammatory cytokines in the colonic homogenates and explants culture. Consistently, CA could interfere with the infiltration and function of mononuclear macrophages in the mucosa, MLNs, and spleens of UC. Furthermore, CA exerted direct suppressive effects on the activation of BMDMs upon the exposure of TLRs agonists in vitro. Taken together, CA could attenuate DSS-induced murine UC through interfering with the activation of macrophages, which might provide an alternative therapeutic option for UC.