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

Anjali Kulkarni-Narla; Bruce Walcheck; David R. Brown

doi:10.1016/S0014-2999(01)00727-0

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

Anjali Kulkarni-Narla
, Bruce Walcheck
, David R. Brown

Veterinary and Biomedical Sciences

Research output: Contribution to journal › Article › peer-review

16 Scopus citations

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 (pIC₅₀ = 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-Ala², N-methyl-Phe⁴, Gly⁵-ol]enkephalin and [D-Pen^2,5]enkephalin albeit with lower potencies. U-50,488H also decreased neutrophil expression of the β₂ 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.

Original language	English (US)
Pages (from-to)	289-294
Number of pages	6
Journal	European Journal of Pharmacology
Volume	414
Issue number	2-3
DOIs	https://doi.org/10.1016/S0014-2999(01)00727-0
State	Published - Mar 2 2001

Bibliographical note

Funding Information:
This investigation was supported by NIH grant DA-10200. A. K.-N. is a postdoctoral fellow supported by NIH Psychoneuroimmunology Training grant T32-07239. The authors thank Mrs. Sheila Alexander for her excellent help and advice in FACS analyses.

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Adhesion
Innate immunity
Integrin
Macrophage inflammatory protein
U-50,488H

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10.1016/S0014-2999(01)00727-0

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title = "Opioid receptors on bone marrow neutrophils modulate chemotaxis and CD11b/CD18 expression",

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 (pIC50 = 10.40 ± 0.61) and inhibited by naloxone (Ke = 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-Ala2, N-methyl-Phe4, Gly5-ol]enkephalin and [D-Pen2,5]enkephalin albeit with lower potencies. U-50,488H also decreased neutrophil expression of the β2 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.",

keywords = "Adhesion, Innate immunity, Integrin, Macrophage inflammatory protein, U-50,488H",

author = "Anjali Kulkarni-Narla and Bruce Walcheck and Brown, \{David R.\}",

note = "Funding Information: This investigation was supported by NIH grant DA-10200. A. K.-N. is a postdoctoral fellow supported by NIH Psychoneuroimmunology Training grant T32-07239. The authors thank Mrs. Sheila Alexander for her excellent help and advice in FACS analyses.",

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doi = "10.1016/S0014-2999(01)00727-0",

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T1 - Opioid receptors on bone marrow neutrophils modulate chemotaxis and CD11b/CD18 expression

AU - Kulkarni-Narla, Anjali

AU - Walcheck, Bruce

AU - Brown, David R.

N1 - Funding Information: This investigation was supported by NIH grant DA-10200. A. K.-N. is a postdoctoral fellow supported by NIH Psychoneuroimmunology Training grant T32-07239. The authors thank Mrs. Sheila Alexander for her excellent help and advice in FACS analyses.

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N2 - 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 (pIC50 = 10.40 ± 0.61) and inhibited by naloxone (Ke = 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-Ala2, N-methyl-Phe4, Gly5-ol]enkephalin and [D-Pen2,5]enkephalin albeit with lower potencies. U-50,488H also decreased neutrophil expression of the β2 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.

AB - 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 (pIC50 = 10.40 ± 0.61) and inhibited by naloxone (Ke = 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-Ala2, N-methyl-Phe4, Gly5-ol]enkephalin and [D-Pen2,5]enkephalin albeit with lower potencies. U-50,488H also decreased neutrophil expression of the β2 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.

KW - Adhesion

KW - Innate immunity

KW - Integrin

KW - Macrophage inflammatory protein

KW - U-50,488H

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U2 - 10.1016/S0014-2999(01)00727-0

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M3 - Article

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JO - European Journal of Pharmacology

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IS - 2-3

ER -

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

Abstract

Bibliographical note

UN SDGs

Keywords

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