Exp Mol Med.  2002 Sep;34(4):308-312.

Vibrio vulnificus cytolysin induces hyperadhesiveness of pulmonary endothelial cells for neutrophils through endothelial P-selectin: a mechanism for pulmonary damage by Vibrio vulnificus cytolysin

Affiliations
  • 1Department of Biochemistry, Chonbuk National University Medical School and Institute of Cardiovascular Research, Chonju, Republic of Korea. jsukim@moak.chonbuk.ac.kr
  • 2Department of Clinical Pathology, Sohae College, Kunsan, Republic of Korea.

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.

Keyword

Vibrio vulnificus cytolysin; P-selectin; endothelial cells; neutrophils

MeSH Terms

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
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