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耶尔森氏菌野生型和突变株在体外和体内对补体活性的调节作用。

Modulation of complement activity in vitro and in vivo by Yersinia wild and mutant strains.

作者信息

Yordanov M, Golkocheva E, Najdenski H

机构信息

Department of Immunology, Institute of Microbiology, Sofia, Bulgaria.

出版信息

Folia Microbiol (Praha). 2006;51(1):27-32. doi: 10.1007/BF02931446.

DOI:10.1007/BF02931446
PMID:16821708
Abstract

The ability of released proteins (Yops) and surface lipopolysaccharides (LPS) from the wild-type strain Yersinia enterocolitica 8081-L2, serotype 0:8 to influence the complement activity was determined. Yops and LPS from wild-type and mutant strains showed different ability to affect the classical pathway (CP) functional complement activity in vitro. The serum CP activity was inhibited during the infection induced with six Y. enterocolitica and three Y. pseudotuberculosis strains in rabbits. The changed complement activity might be of importance for the course of Yersinia infections.

摘要

测定了野生型小肠结肠炎耶尔森菌8081-L2(血清型0:8)释放的蛋白质(Yops)和表面脂多糖(LPS)影响补体活性的能力。野生型和突变株的Yops和LPS在体外影响经典途径(CP)功能性补体活性的能力不同。用六种小肠结肠炎耶尔森菌和三种假结核耶尔森菌菌株感染兔子时,血清CP活性受到抑制。补体活性的改变可能对耶尔森菌感染的病程具有重要意义。

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本文引用的文献

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Lipopolysaccharide O antigen status of Yersinia enterocolitica O:8 is essential for virulence and absence of O antigen affects the expression of other Yersinia virulence factors.小肠结肠炎耶尔森氏菌O:8的脂多糖O抗原状态对其毒力至关重要,且O抗原的缺失会影响其他耶尔森氏菌毒力因子的表达。
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A secreted protein kinase of Yersinia pseudotuberculosis is an indispensable virulence determinant.耶尔森氏假结核杆菌的一种分泌型蛋白激酶是不可或缺的毒力决定因素。
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Isolation of an R- M+ mutant of Yersinia enterocolitica serotype O:8 and its application in construction of rough mutants utilizing mini-Tn5 derivatives and lipopolysaccharide-specific phage.小肠结肠炎耶尔森菌O:8血清型R-M+突变体的分离及其在利用mini-Tn5衍生物和脂多糖特异性噬菌体构建粗糙突变体中的应用。
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Yersinia pseudotuberculosis inhibits Fc receptor-mediated phagocytosis in J774 cells.假结核耶尔森菌抑制J774细胞中Fc受体介导的吞噬作用。
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