Kim Choon-Mee, Park Ra-Young, Chun Ho-Jong, Kim Soo-Young, Rhee Joon-Haeng, Shin Sung-Heui
Research Center for Resistant Cells, Chosun University Medical School, Gwangju, Korea.
FEMS Microbiol Lett. 2007 Apr;269(1):170-9. doi: 10.1111/j.1574-6968.2006.00622.x. Epub 2007 Jan 30.
Bacterial swarming constitutes a good in vitro model for surface adherence and colonization, and is accompanied by expressions of virulence factors related to invasiveness. In this study, it was determined that Vibrio vulnificus swarming was abolished by mutation of the vvpE gene encoding a metalloprotease VvpE and this swarming defect was recovered by complementation of the vvpE gene. Expression of the vvpE gene began simultaneously with the beginning of swarming and increased along with expression of the luxS gene encoding the synthase of the precursor of quorum-sensing signal molecule autoinducer 2, and this increased vvpE expression was decreased by mutation of the luxS gene. Moreover, VvpE destroyed IgA and lactoferrins, which are responsible for mucosal immunity. These results suggest that VvpE may play important roles in the surface adherence and colonization of V. vulnificus by facilitating swarming and in the mucosal invasion of V. vulnificus by destroying IgA and lactoferrin.
细菌群体运动构成了一个用于表面黏附和定植的良好体外模型,并且伴随着与侵袭性相关的毒力因子的表达。在本研究中,已确定编码金属蛋白酶VvpE的vvpE基因突变会消除创伤弧菌的群体运动,并且通过补充vvpE基因可恢复这种群体运动缺陷。vvpE基因的表达与群体运动开始同时启动,并随着编码群体感应信号分子自诱导物2前体合成酶的luxS基因的表达而增加,并且这种增加的vvpE表达会因luxS基因突变而降低。此外,VvpE可破坏负责黏膜免疫的IgA和乳铁蛋白。这些结果表明,VvpE可能通过促进群体运动在创伤弧菌的表面黏附和定植中发挥重要作用,并通过破坏IgA和乳铁蛋白在创伤弧菌的黏膜侵袭中发挥重要作用。