Elucidation of intestinal mucosal immune system through the intracellular processing mechanisms of bacteria and its application for novel therapy of inflammatory bowel disease

我们试图阐明巨噬细胞在肠道炎症中的作用，通过使用IL-10-缺陷（IL-10-/-）小鼠结肠炎模型，并证明异常分化的肠道巨噬细胞亚群通过响应细菌过量产生IL-12和IL-23在Th 1-显性慢性结肠炎中发挥关键作用。此外，我们发现，固有层巨噬细胞（LPMs）可以分为两个子集具有不同的侧散射特性。LPM 2亚群响应于MCP-1而迁移，并且响应于肠道细菌而产生更大量的IL-10。

We tried to elucidate the roles of macrophages in intestinal inflammation by using an IL-10-deficient (IL-10-/-) mouse colitis model, and demonstrated that abnormally differentiated subsets of intestinal macrophage play a key role in Th1-dominant chronic colitis through excess production of IL-12 and IL-23 in response to bacteria. Moreover, we found that lamina propria macrophages (LPMs) could be separated into two subsets with distinct side-scattered properties. LPM2 subset migrated in response to MCP-1 and produced a larger amount of IL-10 in response to commensal bacteria.