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* Speros P. Martel Section of Leukocyte Biology, and
Section of Cardiovascular Sciences, Baylor College of Medicine, Houston, Texas; and
Cox Laboratory for Biomedical Engineering, Rice University, Houston, Texas
Correspondence: C. Wayne Smith, M.D., Section of Leukocyte Biology, Baylor College of Medicine, CNRC, Room 6014, 1100 Bates, Houston, TX 77030-2399. E-mail: cwsmith{at}bcm.tmc.edu
Neutrophils form CD18-dependent adhesions to endothelial cells at sites of inflammation. This phenomenon was investigated under conditions of flow in vitro using isolated human neutrophils and monolayers of HUVEC. The efficiency of conversion of neutrophil rolling to stable adhesion in this model was >95%. Neither anti-CD11a nor anti-CD11b antibodies significantly altered the extent of this conversion, but a combination of both antibodies inhibited the arrest of rolling neutrophils by >95%. The efficiency of transendothelial migration of arrested neutrophils was >90%, and the site of transmigration was typically <6 µm from the site of stationary adhesion. Approximately 70% of transmigrating neutrophils migrated at tricellular corners between three adjacent endothelial cells. A model of neutrophils randomly distributed on endothelium predicted a significantly greater migration distance to these preferred sites of transmigration, but a model of neutrophils adhering to endothelial borders is consistent with observed distances. It appears that stable adhesions form very near tricellular corners.
Key Words: inflammation • adhesion molecules • transmigration
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