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Am J Physiol Regul Integr Comp Physiol 282: R1245-R1252, 2002. First published December 21, 2001; doi:10.1152/ajpregu.00540.2001
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Vol. 282, Issue 4, R1245-R1252, April 2002

L-selectin is required for fMLP- but not C5a-induced margination of neutrophils in pulmonary circulation

Timothy S. Olson1, Kai Singbartl2, and Klaus Ley3

1 Department of Molecular Physiology and Medical Scientist Training Program and 3 Department of Biomedical Engineering and Cardiovascular Research Center, School of Medicine, University of Virginia, Charlottesville, Virginia 22908; and 2 Klinik und Poliklinik für Anästhesiologie und Operative Intensivmedizin, Westfälische Wilhelms-Universität Münster, Münster D-48149, Germany

To study the role of L-selectin in neutrophil (PMN) margination and sequestration in the pulmonary microcirculation, maximally active concentrations of C5a (900 pmol/g) and N-formylmethionyl-leucyl-phenylalanine (fMLP; 0.34 pmol/g) were injected into the jugular vein of wild-type or L-selectin-deficient C57BL/6 mice. In wild-type mice administered C5a or fMLP, 92 ± 1% and 34 ± 9%, respectively, of peripheral blood PMN were trapped mostly in the pulmonary circulation as determined by immunohistochemistry and myeloperoxidase activity. In wild-type mice treated with F(ab')2 fragments of the L-selectin monoclonal antibody MEL-14 or in L-selectin-deficient mice, C5a-induced neutropenia was not significantly reduced, but the decrease in peripheral PMN in response to fMLP was completely abolished, indicating that L-selectin is necessary for fMLP- but not C5a-induced pulmonary margination. Immunostained lung sections of fMLP- or C5a-treated mice showed sequestered neutrophils in alveolar capillaries with no evidence of neutrophil aggregates. We conclude that chemoattractant-induced PMN margination in the pulmonary circulation can occur by two separate mechanisms, one of which requires L-selectin.

formyl peptides; complement; MEL-14; adhesion molecules


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