Colonic macrophages are considered to be major effectors of inflammatory bowel diseases (IBDs) and the control of gut inflammation through C-type lectin receptors is an emerging concept. We show that during colitis, the loss of dectin-1 on myeloid cells prevents intestinal inflammation, while the lack of mannose receptor (MR) exacerbates it. A marked increase in dectin-1 expression in dextran sulfate sodium (DSS)-exposed MR-deficient mice supports the critical contribution of dectin-1 to colitis outcome. Dectin-1 is crucial for Ly6C^highCCR2^high monocyte population enrichment in the blood and their recruitment to inflamed colon as precursors of inflammatory macrophages. Dectin-1 also promotes inflammasome-dependent interleukin-1β (IL-1β) secretion through leukotriene B4 production. Interestingly, colonic inflammation is associated with a concomitant overexpression of dectin-1/CCL2/LTA4H and downregulation of MR on macrophages from IBD patients. Thus, MR and dectin-1 on macrophages are important mucosal inflammatory regulators that contribute to the intestinal inflammation.

结肠巨噬细胞被认为是炎症性肠病（IBD）的主要效应物，通过C型凝集素受体控制肠道炎症是一个新兴的概念。我们表明，在结肠炎期间，髓样细胞上dectin-1的丢失可防止肠道炎症，而缺乏甘露糖受体（MR）则加剧了肠炎。硫酸葡聚糖硫酸钠（DSS）暴露的MR缺陷小鼠中dectin-1表达的显着增加支持了dectin-1对结肠炎结局的关键作用。Dectin-1对于Ly6C^高CCR2^高至关重要单核细胞在血液中的富集及其作为炎性巨噬细胞的前体募集到发炎的结肠中。Dectin-1还通过白三烯B4的产生促进炎症小体依赖性白介素1β（IL-1β）的分泌。有趣的是，结肠炎症与dectin-1 / CCL2 / LTA4H的过表达以及IBD患者巨噬细胞的MR下调相关。因此，巨噬细胞上的MR和dectin-1是重要的粘膜炎症调节剂，有助于肠道炎症。