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Morphine inhibits AP-1 activity and CD14 expression in leukocytes by a nitric oxide and opioid receptor-dependent

I D Welters1, A Menzebach, Y Goumon

  • 1University of liverpool, Division of Clinical Sciences, Liverpool, UK. I.Welters@chiru.med.uni-giessen.de

European Journal of Anaesthesiology
|June 23, 2007
PubMed
Abstract

Insights

Morphine inhibits activator protein 1 (AP-1) activation and CD14 expression in human immune cells via a mu opioid receptor pathway. This suggests a role for morphine in modulating inflammatory responses by affecting AP-1 and CD14.

Area of Science:

  • Immunology
  • Pharmacology
  • Molecular Biology

Background:

  • Activator protein 1 (AP-1) is a key transcription factor regulating proinflammatory mediators.
  • Phagocyte activation by lipopolysaccharide (LPS) is dependent on CD14 cell surface expression.
  • Investigated effects of morphine and nitric oxide on AP-1 and CD14 in human monocytes, neutrophils, and HL-60 cells.

Purpose of the Study:

  • To determine the impact of morphine and nitric oxide on AP-1 activation and CD14 expression.
  • To elucidate the signaling pathways involved in morphine's effects on immune cells.

Main Methods:

  • Human whole blood, monocytes, neutrophils, and HL-60 cells were treated with morphine, nitric oxide donors, or inhibitors.
  • AP-1 nuclear content assessed by flow cytometry and electric mobility shift assay.
  • CD14 expression measured by flow cytometry using fluorescent antibodies.

Main Results:

  • Morphine, followed by LPS stimulation, reduced AP-1 nuclear content in monocytes and neutrophils.
  • Naloxone and nitric oxide synthase inhibitors reversed morphine's inhibitory effects on AP-1.
  • Morphine treatment decreased CD14 expression on neutrophils, an effect also reversed by naloxone and NOS inhibitors.

Conclusions:

  • Morphine inhibits AP-1 activation through a mu opioid receptor pathway involving nitric oxide as a second messenger.
  • Reduced CD14 expression by morphine may contribute to the inhibition of AP-1 activation in LPS-stimulated phagocytes.

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