Adipokine CTRP12 alleviates experimental colitis by participating in modulating mesenteric M2 macrophage polarization in IL-10 KO mice

Purpose Crohn's disease is a chronic inflammatory bowel disease of unknown etiology. Mesentery dysfunction and aberrant adipokine levels participate in the pathogenesis of Crohn's disease. Macrophage polarization plays important roles in mesenteric inflammation. This study aimed to explore the expression of adipokine CTRP12 in Crohn's disease patients and possible roles using IL-10 deficient ( Il-10 ^−/− ) mice. Methods Expression of CTRP12 in mesentery adipose tissue specimens from Crohn's patients(n = 20) and control patients (n = 10) was detected. Il-10 ^−/− mice with established colitis were administered with CTRP12, and untreated mice served as controls (n = 8 for each group). Disease activity, and colonic and mesenteric inflammation was evaluated. Modulation of macrophage polarization and related signaling pathway was also analyzed. Results Our findings indicate CTRP12 is highly expressed in the mesentery of Crohn’s patients. CTRP12 treatment can reduce intestinal and mesenteric inflammation in Crohn’s model mice and can promote the polarization of mesenteric macrophages to M2 type, possibly related to the activation of TGFβRII/Smad signaling pathway. Conclusion These findings suggest adipokine CTRP12 could ameliorate Crohn’s colitis by modulating polarization of mesenteric macrophages to M2 type, providing new target for Crohn’s disease therapy.