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小肠结肠炎耶尔森菌和假结核耶尔森菌与血小板的相互作用。

Interaction of Yersinia enterocolitica and Y. pseudotuberculosis with platelets.

作者信息

Shepel Michael, Boyd Jessica, Luider Joanne, Gibb Alan P

机构信息

*Department of Microbiology & Infectious Diseases, †Department of Pathology & Laboratory Medicine, University of Calgary and ‡Calgary Laboratory Services, Calgary, Canada.

出版信息

J Med Microbiol. 2001 Dec;50(12):1030-1038. doi: 10.1099/0022-1317-50-12-1030.

Abstract

Yersinia enterocolitica is a bacterium capable of growth at 4 degrees C in donated blood and has been responsible for many deaths following transfusion. Interaction of Y. enterocolitica with blood cells is of interest in understanding the mechanisms of survival and growth in blood. The closely related organism Y. pseudotuberculosis is known to invade platelets and cause platelet aggregation by a mechanism that involves expression of the chromosomal inv gene. Yersinia isolates were made to express green fluorescent protein (GFP) and their interaction with platelets was studied by flow cytometry, enterocolitica did not cause platelet aggregation or activation, not even when grown at 22 degrees C to maximise inv expression. Attachment of Y. enterocolitica O:9 to platelets occurred with virulence plasmid-bearing (pYV+) strains grown at 37 degrees C but not with pYV- strains nor with strains grown at 22 degrees C. Y. pseudotuberculosis containing inv did cause platelet activation and aggregation when grown at 22 degrees C, as has been shown before, but also showed enhanced attachment to platelets when grown at 37 degrees C. Electron microscopy studies confirmed that inv-expressing Y. pseudotuberculosis invaded platelets but Y. enterocolitica attached only to the outer surface of platelets. Interaction of Y. enterocolitica O:9 with platelets provided a modest protection against bacterial killing by human serum. Interaction of Y. enterocolitica O:9 with platelets does not lead to platelet invasion or activation, and is mediated through plasmid-coded factors, not inv.

摘要

小肠结肠炎耶尔森菌是一种能够在4摄氏度的献血中生长的细菌,并且已经导致了许多输血后死亡事件。小肠结肠炎耶尔森菌与血细胞的相互作用对于理解其在血液中的存活和生长机制具有重要意义。已知密切相关的假结核耶尔森菌可侵入血小板并通过一种涉及染色体inv基因表达的机制导致血小板聚集。使耶尔森菌分离株表达绿色荧光蛋白(GFP),并通过流式细胞术研究它们与血小板的相互作用,小肠结肠炎耶尔森菌不会导致血小板聚集或激活,即使在22摄氏度生长以最大化inv表达时也不会。小肠结肠炎耶尔森菌O:9与血小板的附着发生在37摄氏度生长的携带毒力质粒(pYV+)的菌株中,但在pYV-菌株或22摄氏度生长的菌株中则不会。如之前所示,含有inv的假结核耶尔森菌在22摄氏度生长时确实会导致血小板激活和聚集,但在37摄氏度生长时也显示出对血小板的附着增强。电子显微镜研究证实,表达inv的假结核耶尔森菌侵入血小板,但小肠结肠炎耶尔森菌仅附着于血小板的外表面。小肠结肠炎耶尔森菌O:9与血小板的相互作用为抵抗人血清对细菌的杀伤提供了一定程度的保护。小肠结肠炎耶尔森菌O:9与血小板的相互作用不会导致血小板侵入或激活,并且是由质粒编码的因子介导的,而不是inv。

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