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Published on: August 16, 2013
[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.
Objective:
Monocytes play a crucial role in the immune response by recognition, ingestion, and intracellular killing of microorganisms. We investigated whether morphine and fentanyl influence CD 11b and CD35 surface receptor expression, phagocytic activity and superoxide anion generation of monocytes in a whole blood flow cytometric assay.
Methods:
Whole blood of 13 healthy volunteers was incubated with different morphine and fentanyl concentrations. Expression of surface receptors CD 11b and CD35 was determined by fluorochrome-labelled antibodies. Phagocytic activity was assessed by ingestion of fluorescent bacteria. Conversion of dihydrorhodamin served for oxidative burst measurements.
Results:
Morphine inhibited monocyte function in a concentration and time dependent manner. Morphine-induced changes were abolished by preincubation with the NO synthase inhibitor N-nitro-l-arginine as well as naloxone. Fentanyl failed to inhibit receptor expression, phagocytosis and reactive oxygen production by monocytes in clinically relevant as well as supraclinical concentrations.
Conclusion:
Our results suggest that these monocyte functions are inhibited by a morphine-stimulated NO release mediated by a mu opiate receptor subtype expressed on the surface of monocytes. In contrast, fentanyl did not share morphine's inhibitory effects on monocyte activity.
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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