Temperature triggers immune evasion by Neisseria meningitidis

摘要

人类病原体"脑膜炎奈瑟菌"能引起败血病和脑膜炎，已形成了各种防御机制，其中包括一种多糖胶囊，它能帮助其在细胞外流体中存活。Christoph Tang及同事在这项研究中发现，对胶囊生物合成所需的三个基因来说，"脑膜炎奈瑟菌"中的胶囊表达是由一个RNA热传感器调控的，后者位于信使RNA的5'－未翻译区域中。作者提出，该细菌通过检测与炎症和免疫效应子的吸纳相关的温度上升来感应鼻咽粘膜的发炎状态。然后，主要采取共生方式的"脑膜炎奈瑟菌"便能够加强其自身的防御，以抵抗宿主对于"共感染病毒病原体"如流感病毒的反应。%Neisseria meningitidis has several strategies to evade complement-mediated killing, and these contribute to its ability to cause septicaemic disease and meningitis. However, the meningococcus is primarily an obligate commensal of the human nasopharynx, and it is unclear why the bacterium has evolved exquisite mechanisms to avoid host immunity. Here we demonstrate that mechanisms of meningococcal immune evasion and resistance against complement increase in response to an increase in ambient temperature. We have identified three independent RNA thermosensors located in the 5' untranslated regions of genes necessary for capsule biosynthesis, the expression of factor H binding protein, and sialylation of lipopolysaccharide, which are essential for meningococcal resistance against immune killing. Therefore increased temperature (which occurs during inflammation) acts as a 'danger signal' for the meningococcus, enhancing its defence against human immune killing. Infection with viral pathogens, such as influenza, leads to inflammation in the nasopharynx with an increased temperature and recruitment of immune effectors. Thermoregulation of immune defence could offer an adaptive advantage to the meningococcus during co-infection with other pathogens, and promote the emergence of virulence in an otherwise commensal bacterium.