Opioid receptors on bone marrow neutrophils modulate chemotaxis and CD11b/CD18 expression.

Abstract:

:Opiates impair neutrophil-mediated host defense, but the involvement of kappa-opioid receptors in this action has not been defined. The selective kappa-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 kappa-opioid receptor agonists bremazocine and ICI-204, 488 also inhibited chemotaxis, as did the respective mu- and delta-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 beta(2) integrin CD11b/CD18 (Mac-1) and adhesion to plastic in a naloxone-reversible manner. The results indicate that kappa-opioid receptors expressed by neutrophils rapidly modulate chemotaxis and adhesion in vitro.

journal_name

Eur J Pharmacol

authors

Kulkarni-Narla A,Walcheck B,Brown DR

doi

10.1016/s0014-2999(01)00727-0

keywords:

subject

Has Abstract

pub_date

2001-03-02 00:00:00

pages

289-94

issue

2-3

eissn

0014-2999

issn

1879-0712

pii

S0014299901007270

journal_volume

414

pub_type

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