Abstract
We observed that normal plasma dramatically reduces neutrophil-endothelial adhesion. Therefore, we identified factors in plasma which might limit PMN adhesion in vitro. We found that the anti-adhesive effect was not mediated by vasoactive lipids present in plasma. Immunoprecipitation of soluble adhesion molecules, P and E-selectins and ICAM-1 restored PMN adhesion to control values. We further examined whether soluble adhesion molecules in plasma might also regulate PMN endothelial migration in response to fMLP (10(-6) M). Plasma significantly reduced PMN migration, and this effect was prevented only by the simultaneous removal of soluble P and E selectins and ICAM-1 together, but not individually. These data show that soluble selectins and ICAM-1 may regulate PMN adhesion and diapedesis, and that alterations in the levels of these molecules may regulate PMN-endothelial interactions in vivo.
MeSH terms
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Adult
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Cell Adhesion / drug effects
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Cell Adhesion / physiology
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Cells, Cultured
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Chemotaxis, Leukocyte / drug effects
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Chemotaxis, Leukocyte / physiology
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E-Selectin / blood
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E-Selectin / physiology
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Endothelium, Vascular / cytology
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Endothelium, Vascular / injuries
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Endothelium, Vascular / physiology*
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Heparin / pharmacology
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Humans
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In Vitro Techniques
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Inflammation Mediators / physiology
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Intercellular Adhesion Molecule-1 / blood
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Intercellular Adhesion Molecule-1 / physiology*
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Lipids / blood
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Lipids / pharmacology
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N-Formylmethionine Leucyl-Phenylalanine / pharmacology
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Neutrophils / cytology
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Neutrophils / drug effects
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Neutrophils / physiology*
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P-Selectin / blood
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P-Selectin / physiology
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Selectins / blood
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Selectins / physiology*
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Solubility
Substances
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E-Selectin
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Inflammation Mediators
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Lipids
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P-Selectin
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Selectins
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Intercellular Adhesion Molecule-1
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N-Formylmethionine Leucyl-Phenylalanine
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Heparin