Department of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
PLoS One. 2010 Dec 23;5(12):e14417. doi: 10.1371/journal.pone.0014417.
Mycoplasma pneumoniae (Mp), a common cause of pneumonia, is associated with asthma; however, the mechanisms underlying this association remain unclear. We investigated the cellular immune response to Mp in mice. Intranasal inoculation with Mp elicited infiltration of the lungs with neutrophils, monocytes and macrophages. Systemic depletion of macrophages, but not neutrophils, resulted in impaired clearance of Mp from the lungs. Accumulation and activation of macrophages were decreased in the lungs of MyD88(-/-) mice and clearance of Mp was impaired, indicating that MyD88 is a key signaling protein in the anti-Mp response. MyD88-dependent signaling was also required for the Mp-induced activation of NFκB, which was essential for macrophages to eliminate the microbe in vitro. Thus, MyD88-NFκB signaling in macrophages is essential for clearance of Mp from the lungs.
肺炎支原体（Mp）是肺炎的常见病因，与哮喘有关；然而，这种关联的机制尚不清楚。我们研究了小鼠对 Mp 的细胞免疫反应。Mp 鼻内接种引起肺部嗜中性粒细胞、单核细胞和巨噬细胞浸润。系统耗尽巨噬细胞，但不耗尽中性粒细胞，导致肺部 Mp 清除受损。MyD88(-/-)小鼠肺部巨噬细胞的积累和激活减少，Mp 的清除受损，表明 MyD88 是抗 Mp 反应中的关键信号蛋白。MyD88 依赖性信号对于 Mp 诱导的 NFκB 激活也是必需的，这对于巨噬细胞在体外清除微生物至关重要。因此，巨噬细胞中的 MyD88-NFκB 信号对于从肺部清除 Mp 是必不可少的。
