Institute of Medical Microbiology and Hospital Hygiene, Heinrich Heine University, Düsseldorf, Germany.
Cell Microbiol. 2012 Feb;14(2):155-67. doi: 10.1111/j.1462-5822.2011.01719.x. Epub 2011 Nov 23.
Bacterial infections cause substantial mortality and burden of disease globally. Induction of a strong innate inflammatory response is the first common host mechanism required for elimination of the invading pathogens. The host transcription factor, nuclear factor kappa B (NF-κB) is essential for immune activation. Conversely, bacterial pathogens have evolved strategies to interfere directly with host cell signalling by regulating or mimicking host proteins. Given the key role of NF-κB in the host inflammatory response, bacteria have expectedly developed virulence effectors interfering with NF-κB signalling pathways. In this review, we explore the bacterial mechanisms utilized to prevent effective NF-κB signalling, which in turn usurp the host inflammatory response.
细菌感染在全球范围内导致了大量的死亡和疾病负担。诱导强烈的先天炎症反应是宿主消除入侵病原体所必需的第一个共同机制。宿主转录因子 NF-κB(核因子 kappa B)对于免疫激活至关重要。相反,细菌病原体已经进化出通过调节或模拟宿主蛋白来直接干扰宿主细胞信号的策略。鉴于 NF-κB 在宿主炎症反应中的关键作用,细菌预计已经开发出了干扰 NF-κB 信号通路的毒力效应因子。在这篇综述中,我们探讨了细菌利用的机制来阻止有效的 NF-κB 信号转导,从而篡夺宿主的炎症反应。