Department of Pathology and Comprehensive Cancer Center, The University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Science. 2012 Jun 8;336(6086):1325-9. doi: 10.1126/science.1222195. Epub 2012 May 10.
The virulence mechanisms that allow pathogens to colonize the intestine remain unclear. Here, we show that germ-free animals are unable to eradicate Citrobacter rodentium, a model for human infections with attaching and effacing bacteria. Early in infection, virulence genes were expressed and required for pathogen growth in conventionally raised mice but not germ-free mice. Virulence gene expression was down-regulated during the late phase of infection, which led to relocation of the pathogen to the intestinal lumen where it was outcompeted by commensals. The ability of commensals to outcompete C. rodentium was determined, at least in part, by the capacity of the pathogen and commensals to grow on structurally similar carbohydrates. Thus, pathogen colonization is controlled by bacterial virulence and through competition with metabolically related commensals.
定植机制使得病原体能够在肠道中定植的机制仍不清楚。在这里，我们表明无菌动物无法根除鼠柠檬酸杆菌，柠檬酸杆菌是一种用于模拟人类附着和消除细菌感染的模型。在感染早期，毒力基因被表达，并需要在常规饲养的小鼠中生长，但在无菌小鼠中不需要。在感染后期，毒力基因的表达下调，导致病原体转移到肠道腔中，在那里它被共生菌所竞争。共生菌竞争柠檬酸杆菌的能力至少部分取决于病原体和共生菌在结构相似的碳水化合物上生长的能力。因此，病原体定植受到细菌毒力和与代谢相关的共生菌竞争的控制。
