人類病原體“腦膜炎奈瑟菌”能引起敗血病和腦膜炎,，已形成了各種防御機制,，其中包括一種多糖膠囊,，它能幫助其在細(xì)胞外流體中存活。Christoph Tang及同事在這項研究中發(fā)現(xiàn),，對膠囊生物合成所需的三個基因來說,，“腦膜炎奈瑟菌”中的膠囊表達(dá)是由一個RNA熱傳感器調(diào)控的，后者位于信使RNA的5′-未翻譯區(qū)域中,。作者提出,，該細(xì)菌通過檢測與炎癥和免疫效應(yīng)子的吸納相關(guān)的溫度上升來感應(yīng)鼻咽粘膜的發(fā)炎狀態(tài)。然后,，主要采取共生方式的“腦膜炎奈瑟菌”便能夠加強其自身的防御,，以抵抗宿主對于“共感染病毒病原體”如流感病毒的反應(yīng),。(生物谷Bioon.com)
生物谷推薦的英文摘要
Nature doi: 10.1038/nature12616
Temperature triggers immune evasion by Neisseria meningitidis
Edmund Loh,Elisabeth Kugelberg,Alexander Tracy,Qian Zhang,Bridget Gollan,Helen Ewles,Ronald Chalmers,Vladimir Pelicic& Christoph M. Tang
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 killing1, 2. 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 effectors3, 4. 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.
