Inflammation of the gastrointestinal tract contributes to the development of inflammatory bowel disease (IBD). Human IBD is modeled by administering dextran sulfate sodium (DSS) to mice. In humans and mice, inflammatory M1 macrophages contribute to the progression of IBD whereas immunosuppressive M2 macrophages protect against colitis. The TLR2/1 agonist PAM3CSK4 (PAM3) induces human and murine monocytes to differentiate into immunosuppressive M2 macrophages, suggesting that PAM3 might be of benefit in the prevention/treatment of colitis. PAM3 was therefore administered to mice treated with DSS. As hypothesized, the number of M2 macrophages rose and disease severity decreased. The critical role of M2 macrophages in this process was established by transferring purified M2 macrophages from PAM3 treated control donors into DSS recipients and reducing colitis. These findings suggest that PAM3 may represent a novel approach to the treatment of human IBD.

胃肠道的炎症有助于炎症性肠病（IBD）的发展。通过将硫酸葡聚糖硫酸钠（DSS）给予小鼠来模拟人IBD。在人类和小鼠中，炎症性M1巨噬细胞可促进IBD的发展，而免疫抑制性M2巨噬细胞可预防结肠炎。TLR2 / 1激动剂PAM3CSK4（PAM3）诱导人和鼠单核细胞分化为免疫抑制性M2巨噬细胞，这表明PAM3可能在预防/治疗结肠炎中有益。因此，将PAM3施用于用DSS治疗的小鼠。如所假设的，M2巨噬细胞的数量增加并且疾病严重性降低。M2巨噬细胞在此过程中的关键作用是通过将纯化的M2巨噬细胞从经过PAM3处理的对照供体转移到DSS受体并减少结肠炎来确立的。这些发现表明，PAM3可能代表了一种治疗人IBD的新方法。