Alkali-treated LPS of Yersinia enterocolitica does not induce expression of E-selectin, ICAM-1 or VCAM-1 on endothelial cells but may mediate antibody- and complement-dependent cell injury.
Lipopolysaccharide (LPS) prepared from a rough mutant of Salmonella typhimurium and deacylated enzymatically (dLPS) does not promote neutrophil adherence to human umbilical vein endothelial cells (HUVECs). This paper reports that similarly, a smooth form of LPS prepared from Yersinia enterocolitica O:3, a serotype known to trigger reactive arthritis in humans, and treated with alkali (yersinia LPS-OH) failed to augment neutrophil adherence to HUVECs. Studies of the mechanism underlying the poor augmentation revealed that neither enzymatically deacylated LPS from Escherichia coli J5 (J5 dLPS) nor yersinia LPS-OH stimulated expression of endothelial cell adhesion molecules E-selectin, VCAM-1 and ICAM-1, whereas both intact J5 LPS and yersinia LPS were stimulatory. Impaired up-regulation could not be explained by decreased binding of yersinia LPS-OH to HUVECs. Furthermore, 51Cr-labelled HUVECs treated with different concentrations of yersinia LPS-OH released 51Cr in the presence of anti-yersinia anti-O antibody and complement. J5 dLPS and yersinia LPS-OH inhibited up-regulation of the adhesion molecules induced by J5 LPS and yersinia LPS but not that induced by tumour necrosis factor alpha. Taken together, the results suggest that although yersinia LPS-OH can depress development of acute inflammation by inhibiting up-regulation of endothelial-cell adhesion molecules, sufficient LPS-OH is bound to induce cell injury and thereby inflammation in the presence of specific antibody and complement. The findings may have pathogenetic implications in yersinia-triggered reactive arthritis characterized by dissemination of yersinia LPS throughout the body.
Repo
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Department of Bacteriology and Immunology, University of Helsinki, Finland.
Renkonen
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Helander
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Leirisalo-Repo
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D000017:ABO Blood-Group System / Q000032:analysis; D000468:Alkalies / Q000494:pharmacology*; D000920:Antibody-Dependent Cell Cytotoxicity / Q000187:drug effects; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000187:drug effects* / Q000502:physiology; D003602:Cytotoxicity, Immunologic / Q000187:drug effects; D019040:E-Selectin; D004730:Endothelium, Vascular / Q000737:chemistry / Q000166:cytology; D004926:Escherichia coli / Q000737:chemistry; D006801:Humans; D018799:Intercellular Adhesion Molecule-1; D008070:Lipopolysaccharides / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D009504:Neutrophils / Q000166:cytology; D014407:Tumor Cells, Cultured; D014471:Umbilical Veins / Q000166:cytology; D015854:Up-Regulation / Q000187:drug effects; D019010:Vascular Cell Adhesion Molecule-1; D015008:Yersinia enterocolitica / Q000737:chemistry*
D000017:ABO Blood-Group System; D000468:Alkalies; D015815:Cell Adhesion Molecules; D019040:E-Selectin; D008070:Lipopolysaccharides; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1