[Morphine inhibits complement receptor expression, phagocytosis and oxidative burst by a nitric oxide dependent

A Menzebach1, J Hirsch, R Nöst

  • 1Abteilung Anästhesiologie, Intensivmedizin und Schmerztherapie, Universitätsklinikum Giessen, Germany.

Abstract

Insights

Morphine impairs monocyte immune functions like phagocytosis by stimulating nitric oxide release. Fentanyl, however, did not affect these critical monocyte activities in the study.

Area of Science:

  • Immunology
  • Pharmacology

Background:

  • Monocytes are vital immune cells responsible for microbial recognition, ingestion, and killing.
  • Opioid analgesics like morphine and fentanyl are widely used, necessitating an understanding of their immunological effects.

Purpose of the Study:

  • To investigate the impact of morphine and fentanyl on monocyte surface receptor expression (CD11b, CD35), phagocytic activity, and superoxide anion generation.
  • To determine if these effects are concentration-dependent and mediated by specific pathways.

Main Methods:

  • Whole blood from healthy volunteers was incubated with varying concentrations of morphine and fentanyl.
  • Monocyte surface receptor expression was analyzed using fluorochrome-labeled antibodies.
  • Phagocytic activity was measured by fluorescent bacteria ingestion.
  • Oxidative burst was assessed via dihydrorhodamine conversion.

Main Results:

  • Morphine significantly inhibited monocyte function in a concentration- and time-dependent manner.
  • Morphine's inhibitory effects were reversed by a nitric oxide synthase inhibitor and naloxone.
  • Fentanyl did not inhibit monocyte receptor expression, phagocytosis, or reactive oxygen production at tested concentrations.

Conclusions:

  • Monocyte function inhibition by morphine appears to be mediated by morphine-stimulated nitric oxide (NO) release via mu-opiate receptors on monocytes.
  • Fentanyl does not exhibit the same inhibitory effects on monocyte activity as morphine.

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