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Research Article Free access | 10.1172/JCI115037

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

C W Smith, T K Kishimoto, O Abbassi, B Hughes, R Rothlein, L V McIntire, E Butcher, D C Anderson, and O Abbass

Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030.

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Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030.

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Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030.

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Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030.

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Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030.

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Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030.

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Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030.

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Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030.

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Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030.

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Published February 1, 1991 - More info

Published in Volume 87, Issue 2 on February 1, 1991
J Clin Invest. 1991;87(2):609–618. https://doi.org/10.1172/JCI115037.
© 1991 The American Society for Clinical Investigation
Published February 1, 1991 - Version history
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Abstract

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

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