Bliska J B, Copass M C, Falkow S
Department of Microbiology, School of Medicine, State University of New York, Stony Brook 11794.
Infect Immun. 1993 Sep;61(9):3914-21. doi: 10.1128/iai.61.9.3914-3921.1993.
We characterized a bacterium-host cell interaction that is mediated by the Yersinia adhesin YadA. Derivatives of the virulence plasmid pIB1 harboring mutations in yadA, yopE, or yopH or in a low-calcium-response regulatory locus were introduced into a Yersinia pseudotuberculosis YPIII strain defective for Inv. The mutant strains were tested for the capacity to attach to and enter HEp-2 cells and express the cytotoxic activities of YopE and YopH. As previously shown, expression of YadA was necessary for bacterial attachment and Yop activity in the absence of Inv (R. Rosqvist, A. Forsberg, M. Rimpilainen, T. Bergman, and H. Wolf-Watz, Mol. Microbiol. 4:657-667, 1990). In addition, bacterial entry into HEp-2 cells occurred efficiently when YadA was expressed in the absence of YopE and YopH. These results demonstrated that YadA mediates intimate attachment of Y. pseudotuberculosis to HEp-2 cells and that phagocytic uptake of bacteria by this pathway is inhibited by the synergistic activities of YopH and YopE. A role for beta 1 integrins as host cell receptors for this bacterial attachment and entry mechanism was supported by HEp-2 cell adhesion and monoclonal antibody neutralization studies.
我们对一种由耶尔森氏菌粘附素YadA介导的细菌与宿主细胞的相互作用进行了表征。将携带yadA、yopE或yopH突变或低钙反应调节位点突变的毒力质粒pIB1衍生物导入对Inv有缺陷的假结核耶尔森氏菌YPIII菌株中。对突变菌株进行了附着和进入HEp-2细胞的能力测试以及YopE和YopH细胞毒性活性的表达测试。如先前所示，在没有Inv的情况下，YadA的表达对于细菌附着和Yop活性是必需的（R. Rosqvist、A. Forsberg、M. Rimpilainen、T. Bergman和H. Wolf-Watz，《分子微生物学》4:657 - 667，1990）。此外，当在没有YopE和YopH的情况下表达YadA时，细菌能有效地进入HEp-2细胞。这些结果表明，YadA介导假结核耶尔森氏菌与HEp-2细胞的紧密附着，并且通过该途径细菌的吞噬摄取受到YopH和YopE协同活性的抑制。HEp-2细胞粘附和单克隆抗体中和研究支持了β1整合素作为这种细菌附着和进入机制的宿主细胞受体的作用。
