Vibrio vulnificus cytolysin induces hyperadhesiveness of pulmonary endothelial cells for neutrophils through endothelial P-selectin: a mechanism for pulmonary damage by Vibrio vulnificus cytolysin.
- Author:
Byeong Soo KIM
1
;
Jong Suk KIM
Author Information
1. Department of Biochemistry, Chonbuk National University Medical School and Institute of Cardiovascular Research, Chonju, Republic of Korea. jsukim@moak.chonbuk.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Vibrio vulnificus cytolysin;
P-selectin;
endothelial cells;
neutrophils
- MeSH:
Animals;
Cattle;
Cell Adhesion/*drug effects;
Cell Line;
Cycloheximide/pharmacology;
Cytotoxins/*toxicity;
Dose-Response Relationship, Drug;
Endothelium, Vascular/cytology/*drug effects/metabolism;
Kinetics;
Neutrophils/*drug effects/pathology;
P-Selectin/*metabolism;
Protein Synthesis Inhibitors/pharmacology;
Pulmonary Artery/cytology/*drug effects/metabolism;
Rats;
Vibrio Infections/etiology/pathology;
Vibrio vulnificus/*pathogenicity
- From:Experimental & Molecular Medicine
2002;34(4):308-312
- CountryRepublic of Korea
- Language:English
-
Abstract:
Vibrio vulnificus cytolysin forms transmembrane pores that are permeable to calcium ions in pulmonary endothelial cells, and has been suggested as an important virulence factor that sequestrate neutrophils primarily in the lung. To elucidate the mechanism we investigated whether the cytolysin affect the expression of endothelial P-selectin and adhesiveness of pulmonary endothelial cells for neutrophils. The cytolysin increased the adhesiveness of CPAE cell, a pulmonary endothelial cell line, for neutrophils in a concentrationand time-dependent manner. The increase of adhesiveness occurred within several minutes after the cytolysin exposure, persisted up to 90 min, and was not affected by cycloheximide. Furthermore, flow cytometric analyses showed that cytolysin enhanced the level of P-selectin on CPAE cell surface. Therefore, these results suggest that the cytolysin-induced hyperadhesiveness of pulmonary endothelial cells for neutrophils is mediated by the mobilization of endothelial P-selectin to the cell surface.
