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小肠结肠炎耶尔森菌和假结核耶尔森菌与胶原蛋白的结合:yopA介导和染色体编码机制的证据。

Binding to collagen by Yersinia enterocolitica and Yersinia pseudotuberculosis: evidence for yopA-mediated and chromosomally encoded mechanisms.

作者信息

Emödy L, Heesemann J, Wolf-Watz H, Skurnik M, Kapperud G, O'Toole P, Wadström T

机构信息

Institute of Medical Microbiology, University of Lund, Sweden.

出版信息

J Bacteriol. 1989 Dec;171(12):6674-9. doi: 10.1128/jb.171.12.6674-6679.1989.

Abstract

Binding of Yersinia enterocolitica and Yersinia pseudotuberculosis strains to type I, II, and IV collagens has been studied. Wild-type strains which harbored the 40- to 50-megadalton virulence plasmid specifically bound all three types of collagen. Curing of the virulence plasmid or Tn5 insertion in the yopA gene encoding the temperature-inducible outer membrane protein YOP1 abolished the binding of all three collagen types to Y. enterocolitica and type I and II collagens to Y. pseudotuberculosis. Full binding capacity was restored by introduction of the yopA gene into nonbinding Yersinia strains. Binding of type I, II, and IV collagens was expressed in Escherichia coli constructs harboring the yopA gene of either Y. enterocolitica or Y. pseudotuberculosis. The interaction of bacterial cells with type I collagen could be blocked by nonradiolabeled native collagens or denatured collagen but not with other serum and connective-tissue proteins. Unlabeled collagen could not displace bound radiolabeled collagen. The binding was inhibited by YOP1-specific polyclonal antibodies, in contrast to normal rabbit serum. The interaction was rapid and was quite resistant to heat treatment, to proteolytic enzymes, to various pHs in both acidic and alkaline ranges, and to the chaotropic agent urea. We propose that this newly identified interaction may be involved both in the first steps of the pathogenesis and in the complications of Yersinia infections affecting connective tissue.

摘要

已对小肠结肠炎耶尔森菌和假结核耶尔森菌菌株与I型、II型和IV型胶原蛋白的结合情况进行了研究。携带40至50兆道尔顿毒力质粒的野生型菌株能特异性结合所有三种类型的胶原蛋白。毒力质粒的消除或编码温度诱导性外膜蛋白YOP1的yopA基因中的Tn5插入,消除了所有三种胶原蛋白类型与小肠结肠炎耶尔森菌的结合以及I型和II型胶原蛋白与假结核耶尔森菌的结合。通过将yopA基因导入无结合能力的耶尔森菌菌株,可恢复其完全结合能力。在携带小肠结肠炎耶尔森菌或假结核耶尔森菌yopA基因的大肠杆菌构建体中表达了I型、II型和IV型胶原蛋白的结合。细菌细胞与I型胶原蛋白的相互作用可被未标记的天然胶原蛋白或变性胶原蛋白阻断,但不能被其他血清和结缔组织蛋白阻断。未标记的胶原蛋白不能取代结合的放射性标记胶原蛋白。与正常兔血清相比,YOP1特异性多克隆抗体可抑制这种结合。这种相互作用迅速,且对热处理、蛋白水解酶、酸性和碱性范围内的各种pH值以及离液剂尿素具有相当的抗性。我们认为,这种新发现的相互作用可能参与了耶尔森菌感染影响结缔组织的发病机制的第一步以及并发症。

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