Inflammatory mediators stimulate granulocyte adherence to cultured human endothelial cells.
The factors that regulate the adherence of granulocytes to the endothelium under normal conditions, and in states of inflammatory vascular injury, are largely unknown. We found that treatment of primary, confluent monolayers of human umbilical vein endothelial cells with inflammatory mediators (zymosan-activated plasma, as a source of C5a fragments, and N-formylmethionyl-leucyl-phenylalanine) stimulated granulocyte adherence to the monolayers. The augmented adherence was dose-, time-, and temperature-related and demonstrated kinetics characteristic of the adherence of single cells with increased affinity for monolayer cultures. Adherence stimulated by the inflammatory mediators was not prevented by washing the monolayers after treatment with the mediator. Human albumin diminished both spontaneous and stimulated adherence, although the relative increase in adherence stimulated by the inflammatory mediator was unchanged. Calcium and magnesium were required for stimulated adherence. These data suggest that inflammatory mediators may bind to, or directly alter, human endothelial cells resulting in enhanced granulocyte adherence, and define characteristics of this endothelial cell-granulocyte interaction.
D002448:Cell Adhesion / Q000187:drug effects; D002478:Cells, Cultured; D003182:Complement C5 / Q000494:pharmacology; D015936:Complement C5a; D004727:Endothelium / Q000276:immunology; D006098:Granulocytes / Q000187:drug effects / Q000276:immunology*; D006801:Humans; D007231:Infant, Newborn; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D010446:Peptide Fragments / Q000494:pharmacology; D014471:Umbilical Veins / Q000276:immunology; D014657:Vasculitis / Q000276:immunology*; D015054:Zymosan / Q000494:pharmacology
D003182:Complement C5; D010446:Peptide Fragments; D009240:N-Formylmethionine Leucyl-Phenylalanine; D015936:Complement C5a; D015054:Zymosan