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Articles in PresS, published online ahead of print December 21, 2001
Am J Physiol Regu Physiol, 10.1152/ajpregu.00540.2001
Submitted on September 5, 2001
Accepted on December 5, 2001
1 Department of Molecular Physiology and Medical Scientist Training Program, University of Virginia, Charlottesville, Virginia, USA
2 Klinik und Poliklinik fur Anasthesiologie und Operative Intensivmedizin, Westfalische Wilhelms-Universitat Munster, Munster, Germany
3 Cardiovascular Research Center and Department of Biomedical Engineering, University of Virginia, Charlottesville, Virginia, USA; Department of Molecular Physiology and Medical Scientist Training Program, University of Virginia, Charlottesville, Virginia, USA
* To whom correspondence should be addressed. E-mail: klausley{at}virginia.edu.
To study the role of L-selectin in neutrophil margination and sequestration in the pulmonary microcirculation, maximally active concentrations of C5a (900 pmol/g) and fMLP (0.34 pmol/g) were injected into the jugular vein of wild-type or L-selectin deficient C57BL6 mice. In wild-type mice, 92 ± 1% (C5a) and 34 ± 9% (fMLP) of peripheral blood neutrophils 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 mAb MEL-14 or in L-selectin-deficient mice, C5a-induced neutropenia was not significantly reduced, but the decrease in peripheral neutrophils in response to fMLP was completely abolished, indicating that L-selectin is necessary for fMLP-, but not C5a-induced pulmonary margination. The discovery of differential requirements for L-selectin raises questions regarding signaling events downstream of receptor engagement by chemoattractants. We conclude that chemoattractant-induced neutrophil margination in the pulmonary circulation can occur by two separate mechanisms, one of which requires L-selectin.
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