Interaction of Yersinia enterocolitica and Y-pseudotuberculosis with platelets

Citation
M. Shepel et al., Interaction of Yersinia enterocolitica and Y-pseudotuberculosis with platelets, J MED MICRO, 50(12), 2001, pp. 1030-1038
Citations number
37
Categorie Soggetti
Microbiology
Journal title
JOURNAL OF MEDICAL MICROBIOLOGY
ISSN journal
00222615 → ACNP
Volume
50
Issue
12
Year of publication
2001
Pages
1030 - 1038
Database
ISI
SICI code
0022-2615(200112)50:12<1030:IOYEAY>2.0.ZU;2-7
Abstract
Yersinia enterocolitica is a bacterium capable of growth at 4 degreesC in d onated blood and has been responsible for many deaths following transfusion . Interaction of Y. enterocolitica with blood cells is of interest in under standing the mechanisms of survival and growth in blood. The closely relate d organism Y pseudotuberculosis is known to invade platelets and cause plat elet 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 now cytometry. Y . enterocolitica did not cause platelet aggregation or activation, not even when grown at 22 degreesC to maximise inv expression. Attachment of Y ente rocolitica O:9 to platelets occurred with virulence plasmid-bearing (pYV(+) ) strains grown at 37 degreesC but not with pYV(-) strains nor with strains grown at 22 degreesC. Y pseudotuberculosis containing inv did cause platel et activation and aggregation when grown at 22 degreesC, as has been shown before, but also showed enhanced attachment to platelets when grown at 37 d egreesC. Electron microscopy studies confirmed that inv-expressing Y. pseud otuberculosis invaded platelets but Y enterocolitica attached only to the o uter surface of platelets. Interaction of Y enterocolitica O:9 with platele ts provided a modest protection against bacterial killing by human serum. I nteraction of Y. enterocolitica O:9 with platelets does not lead to platele t invasion or activation, and is mediated through plasmid-coded factors, no t inv.