Disruption of InlC2 enhances the internalization of Listeria monocytogenes by epithelial cells

作者:Jiang, Jianjun; Chen, Jianshun; Cheng, Changyong; Hu, Hongxia; Bai, Fan; Chen, Ning; Yan, Genqiang; Fang, Weihuan*
来源:WORLD JOURNAL OF MICROBIOLOGY & BIOTECHNOLOGY, 2011, 27(9): 2155-2161.
DOI:10.1007/s11274-011-0681-y

摘要

The LPXTG internlin gene inlC2 is L. monocytogenes specific and formed an internalin cluster with inlD, inlE and, in some cases, inlG between ascB and dapE. Of note, inlC2 was transcribed monocistronically, and of these internalin genes, only inlC2 expression was enhanced in synthetic human gastric fluid. Disruption of inlC2 did not have a polar effect on its downstream internalin genes, but enhanced the production of InlA without changing inlA transcript level, suggesting a link between inlC2 expression and inlA posttranscriptional regulation. The adhesion and invasion rates of Delta inlC2 mutant in epithelial cells were significantly higher than those of parent strain. Also, recovery of listerial cells from the liver and spleen was much higher in mice inoculated with Delta inlC2 mutant than its parent strain. Thus, we speculate that increased invasion of Delta inlC2 mutant into epithelial cells might be due to elevated production of InlA, a major invasin, that could lead further to increased listerial virulence. Overall, this study presents supportive evidence that internalization of L. monocytogenes could be a complex network or unknown mechanisms requiring further study.