致病性耶尔森菌的遗传亲缘关系

А. В. Ушкалов, канд. вет. наук, A. Ushkalov
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引用次数: 0

摘要

这项科研工作致力于研究耶尔森氏菌的遗传亲缘关系。这项工作的目的是归纳有关假结核耶尔森菌、鼠疫耶尔森菌和小肠结肠耶尔森菌之间致病因素和亲缘关系的文献数据。这项研究是通过分析有关假结核耶尔森菌、鼠疫耶尔森菌和小肠结肠炎耶尔森菌之间致病因素和亲缘关系的文献数据进行的。在工作过程中,采用了比较研究法、外显分析法和分析法。使用了国外作者的资料库(Bonacorsi et al:Achtman 等人,2004 年;Abreu-Goodger & Merino,2005 年;Wagner 等人,2014 年;Santos-Montañez 等人,2015 年)以及其他许多对这一问题进行研究并将结果反映在其研究著作中的作者。目前已确定耶尔森菌的 "致病性武器库 "包括多种粘附素,可使入侵的病原体在宿主体内立足,并在感染后期附着在某些组织上。当宿主的先天免疫系统被激活时,这三种病原体都会产生一种类似于注射用医用针头的结构。结合在宿主细胞膜上形成孔隙的转座子,所形成的通道可确保将六种 "效应 "蛋白转移到宿主细胞的细胞质中。这些蛋白质模仿宿主细胞的蛋白质,但在改变宿主细胞的细胞骨架、诱导宿主细胞凋亡方面比本地蛋白质更有效。这样一个复杂的武器库确保了尽管宿主竭尽全力抵御病原体的感染,但 禺尔丝菌仍能保持优势。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
GENETIC RELATEDNESS OF PATHOGENIC YERSINIA
The scientific work is devoted to the study of genetic relatedness of Yersinia bacterial species. The purpose of the work is to generalize literature data on pathogenicity factors and relatedness between Yersinia pseudotuberculosis, Y. pestis and Y. enterocolitica. The research was carried out by analyzing data from the literature regarding pathogenicity factors and relatedness between Yersinia pseudotuberculosis and Y. pestis and Y. enterocolitica. During the execution of the work, a comparative method of research, episiotic, and analysis was used. Used the source base of foreign authors (Bonacorsi et al., 1994: Achtman et al., 2004; Abreu-Goodger & Merino, 2005; Wagner et al., 2014; Santos-Montañez et al., 2015) and many others who conducted research on this issue and reflected the results in their research works. It has been established that Yersinia's «arsenal of pathogenicity» includes a number of adhesins that allow invading pathogens to establish themselves in the host and attach to certain tissues later in the course of infection. When the host's innate immune system is activated, all three pathogens produce a structure similar to a medical needle for injection. In combination with the translocon, which forms a pore in the host membrane, the formed channel ensures the transfer of six «effector» proteins into the cytoplasm of the host cell. These proteins mimic host cell proteins but are more efficient than their native counterparts in modifying the host cell cytoskeleton, inducing host cell apoptosis. Such a complex arsenal ensures that уersinia maintain an advantage, despite all the efforts of the host to counteract the infecting pathogen.
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