Center of Chronic Immunodeficiency, University of Freiburg, 79106 Freiburg, Germany.
J Immunol. 2012 Jan 15;188(2):774-80. doi: 10.4049/jimmunol.1101383. Epub 2011 Dec 19.
Group B streptococci, a major cause of sepsis, induce inflammatory cytokines in strict dependence on bacterial ssRNA and the host molecules MyD88 and UNC-93B. In this study, we show that NO plays an important role in Group B streptococci-induced transcriptional activation of cytokine genes. Phagocytosis induced NO in a MyD88-dependent fashion. In turn, NO propagated the acidification of phagosomes and the processing of phagosomal bacterial nucleic acids and was required for potent transcriptional activation of cytokine genes by streptococci. This NO-dependent amplification loop has important mechanistic implications for the anti-streptococcal macrophage response and sepsis pathogenesis.
B 群链球菌是败血症的主要病因之一,其严格依赖于细菌 ssRNA 以及宿主分子 MyD88 和 UNC-93B 来诱导炎症细胞因子的产生。在本研究中,我们发现一氧化氮(NO)在 B 群链球菌诱导细胞因子基因转录激活中发挥重要作用。吞噬作用以 MyD88 依赖的方式诱导产生 NO。反过来,NO 促进了吞噬体的酸化以及吞噬体中细菌核酸的加工,这对于链球菌强有力地激活细胞因子基因的转录是必需的。这种依赖于 NO 的扩增环对于抗链球菌的巨噬细胞反应和脓毒症发病机制具有重要的机制意义。