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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Hentzen, E. R. Articles by Simon, S. I. Search for Related Content PubMed PubMed Citation Articles by Hentzen, E. R. Articles by Simon, S. I. Related Collections Hemostasis, Thrombosis, and Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, Vol. 95 No. 3 (February 1), 2000: pp. 911-920 Sequential binding of CD11a/CD18 and CD11b/CD18 defines neutrophil capture and stable adhesion to intercellular adhesion molecule-1 Eric R. Hentzen, Sriram Neelamegham, Geoffrey S. Kansas, Jennifer A. Benanti, Larry V. McIntire, C. Wayne Smith, and Scott I. Simon From the Speros Martel Section of Leukocyte Biology, Department of Pediatrics, Baylor College of Medicine, Houston, TX; The Cox Laboratory for Biomedical Engineering, Institute of Biosciences and Bioengineering, Rice University, Houston, TX; Department of Chemical Engineering, State University of New York, Buffalo, NY; and the Department of Microbiology and Immunology, Northwestern University Medical School, Chicago, IL. The relative contributions of CD11a/CD18 and CD11b/CD18 to the dynamics and strength of neutrophil adhesion to intercellular adhesion molecule (ICAM)-1-transfected cells were examined over the time course of chemotactic stimulation. Suspensions of neutrophils and transfectants were sheared in a cone-plate viscometer, and formation of heterotypic aggregates was measured by 2-color flow cytometry. The 2-body collision theory was used to compute adhesion efficiency, defined as the proportion of collisions between neutrophils and target cells that resulted in capture. ICAM-1 surface density and shear rate both regulated adhesion efficiency. Target cells expressing approximately 1000 ICAM-1 sites/µm2 (Ilow) were captured with an efficiency of 0.15 at 100 s1, which decreased to zero at 300 s1. At 8-fold higher ICAM-1 expression (Ihigh) corresponding to levels measured on interleukin-1-stimulated endothelium, efficiency was 0.3 at 100 s1 and remained above background to 900 s1. Shear alone was sufficient for CD11a/CD18-mediated adhesion to ICAM-1, and stimulation with formyl-methionyl-leucyl-phenylalanine boosted capture efficiency through CD11a/CD18 by 4-fold. In comparison, CD11b/CD18 supported one third of this efficiency, but was necessary for aggregate stability over several minutes of shear and at shear stresses exceeding 5 dyne/cm2. Hydrodynamics influenced capture efficiency predominantly through the collisional contact duration, predicted to be approximately 9 milliseconds for successful capture of Ilow and 4 milliseconds for Ihigh. The implication is that an increase in ICAM-1 from resting levels to those on inflamed endothelium effectively increases the permissible shear in which capture through 2-integrins may occur. Neutrophil adhesion to ICAM-1 appears to be a cooperative and sequential process of CD11a-dependent capture followed by CD11b-mediated stabilization. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Liang, C. Fu, D. Wagner, H. Guo, D. Zhan, C. Dong, and M. Long Two-dimensional kinetics of {beta}2-integrin and ICAM-1 bindings between neutrophils and melanoma cells in a shear flow Am J Physiol Cell Physiol, March 1, 2008; 294(3): C743 - C753. [Abstract] [Full Text] [PDF] P. F. Bradfield, C. A. Johnson-Leger, C. 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