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Inhibition of phagocytosis in Yersinia pseudotuberculosis: a virulence plasmid-encoded ability involving the Yop2b protein.

机译:吞噬假结核耶尔森氏菌中的吞噬作用的抑制:一种毒性质粒编码能力涉及Yop2b蛋白。

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摘要

Virulence plasmid-containing cells of Yersinia pseudotuberculosis had the ability to inhibit phagocytosis by mouse peritoneal macrophages cultured in vitro, but cells of its plasmid-cured derivative did not. Inhibition was most pronounced when the pathogen was incubated under Ca2+-deficient conditions, which allowed a high level of expression of outer membrane proteins (Yops). The addition of 2.5 mM Ca2+ to the growth medium reduced the degree of inhibition by the pathogen, but it was still significantly higher than that of the plasmid-cured strain. An avirulent mutant strain, from which the entire yopH gene was deleted, was impaired in its phagocytosis inhibition ability. This mutant could be trans-complemented by the yopH+ gene back to the wild-type phenotype with respect to virulence, as well as the ability to inhibit phagocytosis, demonstrating that the ability to inhibit phagocytosis is an important virulence function. The mutant strain was still cytotoxic for HeLa cells, indicating that inhibition of phagocytosis can be genetically separated from the ability to cause a cytotoxic effect.
机译:含有致病性假结核耶尔森氏菌质粒的细胞具有抑制体外培养的小鼠腹膜巨噬细胞吞噬作用的能力,但其质粒固化衍生物的细胞却没有。当病原体在缺乏Ca2 +的条件下孵育时,抑制作用最为明显,这使得外膜蛋白(Yops)的表达水平很高。向生长培养基中添加2.5 mM Ca2 +可以降低病原体的抑制程度,但仍远高于质粒固化菌株。删除了整个yopH基因的无毒突变株,其吞噬作用抑制能力受损。就毒性而言,该突变体可以由yopH +基因反式补充为野生型表型,并具有抑制吞噬作用的能力,这表明抑制吞噬作用的能力是重要的毒力功能。突变株对HeLa细胞仍然具有细胞毒性,表明对吞噬作用的抑制可从遗传上与引起细胞毒性作用的能力区分开。

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