首页> 外文期刊>Infection and immunity >Plasmid-mediated surface fibrillae of Yersinia pseudotuberculosis and Yersinia enterocolitica: relationship to the outer membrane protein YOP1 and possible importance for pathogenesis.
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Plasmid-mediated surface fibrillae of Yersinia pseudotuberculosis and Yersinia enterocolitica: relationship to the outer membrane protein YOP1 and possible importance for pathogenesis.

机译:质粒介导的耶尔森氏菌假结核耶尔森氏菌和小肠结肠炎耶尔森氏菌的表面原纤维:与外膜蛋白YOP1的关系和可能的发病机理。

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The cell surface properties of Yersinia pseudotuberculosis and Yersinia enterocolitica mutants, constructed by insertional inactivation of genes located on the 40- to 50-megadalton virulence plasmid, were examined. Electron microscopy revealed an absolute correlation between expression of four plasmid-dependent, temperature-inducible properties related to the bacterial surface: (i) a fibrillar matrix covering the outer membrane, (ii) outer membrane protein YOP1, (iii) spontaneous autoagglutination, and (iv) mannose-resistant hemagglutination of guinea pig erythrocytes. Immunoelectron microscopy indicated that YOP1 is a structural component of the fibrillae. Experiments demonstrating inhibition of hemagglutination by anti-YOP1 monoclonal antibody suggested a potential role for YOP1 in adhesion. Insertional inactivation of the gene coding for YOP1, with resultant loss of the ability to express fibrillae, led to a significant reduction in the capacity of Y. enterocolitica, but not Y. pseudotuberculosis, to colonize the ileum of orogastrically infected mice. In both Y. enterocolitica and Y. pseudotuberculosis, inactivation of the genes coding for Ca2+ dependency reduced the ability to maintain intestinal colonization, regardless of the ability to express fibrillae. Both surface fibrillae and Ca2+ dependency seem to reflect pathogenic determinants which are required for the establishment of Y. enterocolitica infection. In Y. pseudotuberculosis, however, no clinical significance of the fibrillae has so far been defined.
机译:检查了耶尔森氏菌假结核耶尔森氏菌和小肠结肠炎耶尔森氏菌突变体的细胞表面特性,这些突变体是通过插入灭活40至50兆道尔顿毒力质粒上的基因而构建的。电子显微镜显示与细菌表面有关的四个质粒依赖性温度诱导特性的表达之间存在绝对相关性:(i)覆盖外膜的纤维状基质,(ii)外膜蛋白YOP1,(iii)自发自发凝集,和(iv)豚鼠红细胞的抗甘露糖血凝反应。免疫电子显微镜检查表明,YOP1是原纤维的结构成分。证明抗YOP1单克隆抗体抑制血凝的实验表明,YOP1在黏附中具有潜在作用。编码YOP1的基因的插入失活,导致丧失表达原纤维的能力,导致肠道小肠结肠炎耶尔森菌(而非假结核耶尔森氏菌)定殖于经胃胃感染的小鼠回肠的能力显着降低。在小肠结肠炎耶尔森氏菌和假结核耶尔森氏菌中,编码Ca2 +依赖性基因的失活都会降低维持肠道菌落的能力,而与表达原纤维的能力无关。表面原纤维和Ca 2+依赖性似乎都反映了建立小肠结肠炎耶尔森氏菌感染所需的致病性决定因素。然而,在假结核耶尔森氏菌中,迄今尚未确定原纤维的临床意义。

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