英国一项最新研究说，沙门氏菌在感染细胞时采取了严格的“三步走”战略，这一发现有助研发针对沙门氏菌的新药物。
英国帝国理工学院研究人员在新一期美国《科学》杂志上报告说，他们研究发现，沙门氏菌细胞在感染目标细胞时遵循以下步骤：首先，在自己表面形成一个针状突起，以此建立和目标细胞之间的接触；然后，一些专门的蛋白质会通过这个突起抵达目标细胞，破坏目标细胞的细胞膜，打出一个“洞口”；最后，沙门氏菌细胞通过“洞口”向目标细胞释放真正具有毒性的蛋白质。
领导研究的戴维·霍尔登教授说，沙门氏菌这样做，可以保证感染的成功率。
沙门氏菌导致的沙门氏菌病是一种常见的通过污染食物传播的疾病。患者的临床表现包括头痛、恶心、腹痛、呕吐、腹泻、发热等。
研究人员希望，在探明沙门氏菌感染目标细胞的机制后，可以研发出更有效的药物或疫苗。(生物谷Bioon.com)
生物谷推荐原文出处：
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.
