Hensler Mary E, Liu George Y, Sobczak Susan, Benirschke Kurt, Nizet Victor, Heldt Gregory P
Department of Pediatrics, Division of Infectious Diseases, School of Medicine, University of California at San Diego, La Jolla, California 92093-0687, USA.
J Infect Dis. 2005 Apr 15;191(8):1287-91. doi: 10.1086/428946. Epub 2005 Mar 10.
We examined the virulence role of group B Streptococcus (GBS) beta-hemolysin/cytolysin (beta h/c) in a neonatal-rabbit model of GBS pulmonary infection. Rabbits infected intratracheally with wild-type (wt) GBS developed focal pneumonia and, by 18 h after infection, had 100-fold more bacteria in lung tissue than did rabbits infected with a delta beta h/c mutant. Mortality (40% vs. 0%), development of bacteremia, and mean bacterial blood counts were all significantly higher in the rabbits challenged with wt GBS than in those challenged with the delta beta h/c mutant. Lung compliance during mechanical ventilation was impaired after injection of wt GBS but not after injection of the Delta beta h/c mutant strain. This work, to our knowledge, provides the first in vivo evidence for a critical role of the beta h/c toxin in GBS neonatal pneumonia and in the breakdown of the pulmonary barrier to systemic infection.
我们在B族链球菌(GBS)肺部感染的新生兔模型中研究了GBSβ-溶血素/细胞毒素(βh/c)的毒力作用。经气管内感染野生型(wt)GBS的兔子发生了局灶性肺炎,并且在感染后18小时,其肺组织中的细菌数量比感染βh/c缺失突变体的兔子多100倍。用wt GBS攻击的兔子的死亡率(40%对0%)、菌血症的发生情况以及平均细菌血计数均显著高于用βh/c缺失突变体攻击的兔子。注射wt GBS后机械通气期间的肺顺应性受损,但注射βh/c缺失突变体菌株后未受损。据我们所知,这项工作首次在体内证明了βh/c毒素在GBS新生儿肺炎以及肺部屏障对全身感染的破坏中起关键作用。