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Significance Inflammatory bowel disease (IBD) can be debilitating, and sometimes leads to life-threatening complications. Macrophages play a critical role in colitis by secreting many cytokines and regulating tissue repair. Here, we provide evidence showing that the IBD susceptibility geneECM1 is critical for controlling colonic inflammation through macrophages in colitis.ECM1 deficiency in macrophages resulted in reduced sensitivity to dextran sodium sulphate-induced colitis with increased expression of granulocyte-macrophage colony-stimulating factor (GM-CSF)-promoted arginase 1 and impaired M1 polarization by activating the STAT5 pathway. These results reveal a function of the IBD susceptibility geneECM1 in colonic macrophages through GM-CSF/STAT5 regulatory axis and indicate that the attenuation of ECM1 function in macrophages is a potential strategy for IBD therapy.

ECM1 is an essential factor for the determination of M1 macrophage polarization in IBD in response to LPS stimulation