HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by St. Hill, C. A. Articles by Walcheck, B. Search for Related Content PubMed PubMed Citation Articles by St. Hill, C. A. Articles by Walcheck, B.

(Journal of Leukocyte Biology. 2003;73:464-471.)
© 2003 by Society for Leukocyte Biology

Indirect capture augments leukocyte accumulation on P-selectin in flowing whole blood

The Center for Immunology and the Departments of Veterinary PathoBiology and Laboratory Medicine and Pathology, University of Minnesota Academic Health Center, University of Minnesota, St. Paul

Correspondence: Dr. Bruce Walcheck, University of Minnesota, 295j, AS/VM Bldg., 1988 Fitch Ave., St. Paul, MN 55108. E-mail: walch003{at}umn.edu

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.

Key Words: inflammation • L-selectin • margination

This article has been cited by other articles:

				Z. Ni, J. J. Campbell, G. Niehans, and B. Walcheck The Monoclonal Antibody CHO-131 Identifies a Subset of Cutaneous Lymphocyte-Associated Antigen T Cells Enriched in P-Selectin-Binding Cells J. Immunol., October 1, 2006; 177(7): 4742 - 4748. [Abstract] [Full Text] [PDF]

				Y. Li, J. Brazzell, A. Herrera, and B. Walcheck ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding Blood, October 1, 2006; 108(7): 2275 - 2279. [Abstract] [Full Text] [PDF]

				P. E. Mattila, C. E. Green, U. Schaff, S. I. Simon, and B. Walcheck Cytoskeletal interactions regulate inducible L-selectin clustering Am J Physiol Cell Physiol, August 1, 2005; 289(2): C323 - C332. [Abstract] [Full Text] [PDF]

				M. M. Burdick and K. Konstantopoulos Platelet-induced enhancement of LS174T colon carcinoma and THP-1 monocytoid cell adhesion to vascular endothelium under flow Am J Physiol Cell Physiol, August 1, 2004; 287(2): C539 - C547. [Abstract] [Full Text] [PDF]

				B. Walcheck, S. R. Alexander, C. A. St. Hill, and E. Matala ADAM-17-independent shedding of L-selectin J. Leukoc. Biol., September 1, 2003; 74(3): 389 - 394. [Abstract] [Full Text] [PDF]