Chemotactic factors regulate lectin adhesion molecule 1 (LECAM-1)-dependent neutrophil adhesion to cytokine-stimulated endothelial cells in vitro.

摘要: Monoclonal antibodies recognizing CD18, CD11a, CD11b, and neutrophil lectin adhesion molecule 1 (LECAM-1), i.e., the human homologue of murine MEL-14 antigen, were used to assess relative contribution these glycoproteins neutrophil-endothelial adhesion. Under static conditions, neutrophils IL-1-stimulated umbilical vein endothelial cell (HUVEC) monolayers was inhibited by LECAM-1, effect combining anti-LECAM-1 anti-CD11a almost additive. flow at a wall shear stress 1.85 dyn/cm2, condition where CD18-dependent is minimal, greater than 50%. Chemotactic stimulation induced rapid loss LECAM-1 from surface, level surface closely correlated with under flow. Neutrophils contacting activated cells for 30 min lost much their phenomenon soluble factor or factors released into medium stimulated monolayers, high percentage migrated through HUVEC monolayer. This migration completely anti-CD18, but unaffected LECAM-1. These results support concept that participates in adherence unstimulated cytokine-stimulated conditions flow, then coincident engagement mechanisms leading transendothelial migration.