Department of Laboratory Animal Medicine, College of Veterinary Medicine, Konkuk University, Seoul 143-701, Republic of Korea.
J Microbiol. 2011 Dec;49(6):1050-3. doi: 10.1007/s12275-011-1043-z. Epub 2011 Dec 28.
We report, herein, an attempt to determine whether an IL-10-induced immunological state affects the response of macrophages against Salmonella Typhimurium (ST). Pretreatment with mrIL-10 induced the intracellular invasion of ST into macrophages in a dose-dependent manner. It also activated AKT phosphorylation, cyclin D1, Bcl-X(L), and COX-2 upon ST infection, which may correlate with Salmonella's survival within the macrophages. However, I-κB phosphorylation was shown to be inhibited, along with the expression of TNF-α and MIP-2α mRNA. Therefore, IL-10 not only suppresses the bactericidal response of macrophages against ST, but also ultimately causes infected macrophages to function as hosts for ST replication.
我们在此报告,试图确定白细胞介素-10(IL-10)诱导的免疫状态是否会影响巨噬细胞对沙门氏菌 Typhimurium(ST)的反应。用 mrIL-10 预处理会以剂量依赖的方式诱导 ST 进入巨噬细胞的细胞内入侵。它还会在 ST 感染时激活 AKT 磷酸化、细胞周期蛋白 D1、Bcl-X(L)和 COX-2,这可能与沙门氏菌在巨噬细胞内的存活有关。然而,已经表明 I-κB 磷酸化被抑制,同时 TNF-α 和 MIP-2α mRNA 的表达也被抑制。因此,IL-10 不仅抑制了巨噬细胞对 ST 的杀菌反应,而且最终使受感染的巨噬细胞成为 ST 复制的宿主。