Abstract
Opiates impair neutrophil-mediated host defense, but the involvement of κ-opioid receptors in this action has not been defined. The selective κ-opioid receptor agonist [ trans-(+)3,4-dichloro- N-methyl- N[2-(1-pyrrolidinyl)-cyclohexyl]benzeneacetamide methanesulfonate inhibited macrophage inflammatory protein-2-induced chemotaxis of bone marrow neutrophils from C57BL/6 mice. Its effects were concentration-dependent ( pIC 50=10.40±0.61) and inhibited by naloxone ( K e=0.27 nM). The κ-opioid receptor agonists bremazocine and ICI-204, 488 also inhibited chemotaxis, as did the respective μ- and δ-opioid receptor agonists [ d-Ala 2, N-methyl-Phe 4, Gly 5-ol]enkephalin and [ d-Pen 2,5]enkephalin albeit with lower potencies. U-50,488H also decreased neutrophil expression of the β 2 integrin CD11b/CD18 (Mac-1) and adhesion to plastic in a naloxone-reversible manner. The results indicate that κ-opioid receptors expressed by neutrophils rapidly modulate chemotaxis and adhesion in vitro.
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