Isberg R R
Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts 02111.
Infect Immun. 1989 Jul;57(7):1998-2005. doi: 10.1128/iai.57.7.1998-2005.1989.
Yersinia pseudotuberculosis inv mutants were analyzed for their ability to bind and penetrate mammalian cell lines. Strains defective for the production of invasin and cured of the Yersinia virulence plasmid pIB1 were extremely defective for entry into the HEp-2 cell line. inv strains harboring the virulence plasmid partially overcame this defect, indicating that the virulence plasmid mediates an invasin-independent pathway for low-level entry into cultured cells. Plasmid-cured inv mutants were able to attach efficiently to mammalian cells after bacterial culture at 37 degrees C but not after culture at a lower temperature. The enhanced cellular binding of inv mutants grown at 37 degrees C did not result in efficient cellular penetration, indicating that invasin-mediated entry is the primary chromosomally encoded pathway responsible for Y. pseudotuberculosis penetration into both HEp-2 and Chinese hamster ovary cells under the assay conditions described here.
对耶尔森氏假结核菌inv突变体结合和穿透哺乳动物细胞系的能力进行了分析。缺失侵袭素产生且已治愈耶尔森氏菌毒力质粒pIB1的菌株在进入HEp - 2细胞系方面存在极大缺陷。携带毒力质粒的inv菌株部分克服了这一缺陷,表明毒力质粒介导了一条不依赖侵袭素的低水平进入培养细胞的途径。质粒治愈的inv突变体在37摄氏度细菌培养后能够有效地附着于哺乳动物细胞,但在较低温度培养后则不能。在37摄氏度生长的inv突变体增强的细胞结合并未导致有效的细胞穿透,这表明在本文所述的检测条件下,侵袭素介导的进入是负责耶尔森氏假结核菌进入HEp - 2和中国仓鼠卵巢细胞的主要染色体编码途径。