英國一項最新研究說,，沙門氏菌在感染細胞時采取了嚴格的“三步走”戰(zhàn)略,，這一發(fā)現(xiàn)有助研發(fā)針對沙門氏菌的新藥物。
英國帝國理工學院研究人員在新一期美國《科學》雜志上報告說,，他們研究發(fā)現(xiàn),，沙門氏菌細胞在感染目標細胞時遵循以下步驟：首先，在自己表面形成一個針狀突起,，以此建立和目標細胞之間的接觸,；然后，一些專門的蛋白質會通過這個突起抵達目標細胞,，破壞目標細胞的細胞膜,，打出一個“洞口”；最后,，沙門氏菌細胞通過“洞口”向目標細胞釋放真正具有毒性的蛋白質,。
領導研究的戴維·霍爾登教授說，沙門氏菌這樣做,，可以保證感染的成功率,。
沙門氏菌導致的沙門氏菌病是一種常見的通過污染食物傳播的疾病,?；颊叩呐R床表現(xiàn)包括頭痛、惡心,、腹痛,、嘔吐、腹瀉,、發(fā)熱等,。
研究人員希望，在探明沙門氏菌感染目標細胞的機制后,，可以研發(fā)出更有效的藥物或疫苗,。(生物谷Bioon.com)
生物谷推薦原文出處：
Science DOI: 10.1126/science.1189000
pH Sensing by Intracellular Salmonella Induces Effector Translocation
Xiu-Jun Yu, Kieran McGourty, Mei Liu, Kate E. Unsworth,* David W. Holden
Salmonella enterica is an important intracellular bacterial pathogen of humans and animals. It replicates within host cell vacuoles by delivering virulence (effector) proteins through a vacuolar membrane pore made by the SPI-2 type III secretion system (T3SS). T3SS assembly follows vacuole acidification, but when bacteria are grown at low pH, effector secretion is negligible. Here, we found that effector secretion was activated at low pH from mutant strains lacking a complex of SPI-2–encoded proteins SsaM, SpiC, and SsaL. Exposure of wild-type bacteria to pH 7.2 after growth at pH 5.0 caused dissociation and degradation of SsaM/SpiC/SsaL complexes and effector secretion. In infected cells, loss of the pH 7.2 signal by acidification of host cell cytosol prevented complex degradation and effector translocation. Thus, intravacuolar Salmonella senses host cytosolic pH, resulting in degradation of regulatory complex proteins and effector translocation.
Section of Microbiology, Centre for Molecular Microbiology and Infection, Imperial College London, Armstrong Road, London SW7 2AZ, UK.
