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Indirect capture augments leukocyte accumulation on P‐selectin in flowing whole blood
Author(s) -
St. Hill Catherine A.,
Alexander Shelia R.,
Walcheck Bruce
Publication year - 2003
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1002491
Subject(s) - biology , p selectin , inflammation , immunology , leukocyte trafficking , whole blood , monoclonal antibody , endothelium , l selectin , platelet , microbiology and biotechnology , blood cell , antibody , cell adhesion molecule , platelet activation , chemokine , endocrinology
Leukocytes are captured directly by E‐ and P‐selectin on activated endothelium and by indirect means, which includes attached leukocytes capturing free‐flowing leukocytes. However, controversy exists as to whether the latter mechanism occurs in the presence of red blood cells. We analyzed leukocyte capture mechanisms on P‐selectin under circulatory hydrodynamics using whole blood. The selective disruption of leukocyte–leukocyte interactions with an L‐selectin monoclonal antibody reduced leukocyte accumulation by >50% under various stringencies (substrate concentrations and shear stresses). In addition, a direct analysis of leukocyte capture events revealed that 69% were indirect. Our data indicate that in the presence of red blood cells, P‐selectin‐attached leukocytes, individually and as a monolayer, augment leukocyte accumulation by indirect capture. This mechanism may contribute to increasing the density of leukocytes on discrete areas of activated endothelial cells at sites of inflammation. These findings are significant since L‐selectin accounts for the majority of the leukocyte rolling flux in small venules at diverse inflammatory settings. Yet, the primary mechanism by which L‐selectin mediates leukocyte accumulation remains unresolved.