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Morphine reciprocally regulates IL-10 and IL-12 production by monocyte-derived human dendritic cells and enhances T

Davorka Messmer1, Ikusuke Hatsukari, Naoko Hitosugi

  • 1Laboratory of Experimental Immunology, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY, USA. dmessmer@ucsd.edu

Molecular Medicine (Cambridge, Mass.)
|March 24, 2007
PubMed

Insights

Morphine enhances the immune response by modulating dendritic cell (DC) maturation. This opioid receptor activation boosts T cell stimulation, indicating an immunostimulatory effect.

Area of Science:

  • Immunology
  • Pharmacology
  • Cell Biology

Background:

  • Dendritic cells (DCs) are key immune regulators.
  • Opioid receptors (mu, kappa, delta) are expressed on immune cells.
  • Morphine's immunomodulatory effects are not fully understood.

Purpose of the Study:

  • To investigate the effect of morphine on human dendritic cell (DC) development and function.
  • To determine if morphine influences DC maturation and T cell stimulatory capacity.

Main Methods:

  • Human monocytes were differentiated into DCs in the presence of varying concentrations of morphine.
  • LPS-induced maturation markers (HLA-DR, CD86, CD80, CD83) and cytokine secretion (IL-10, IL-12) were analyzed.
  • T cell stimulatory capacity was assessed, and the role of opioid receptors was examined using naloxone.

Main Results:

  • Immature DCs expressed mu, kappa, and delta opioid receptors.
  • Chronic morphine treatment augmented LPS-induced upregulation of DC maturation markers.
  • Morphine increased DC T cell stimulatory capacity, decreased IL-10, and increased IL-12 secretion in a p38 MAPK-dependent manner.
  • Naloxone reversed the effects of morphine.

Conclusions:

  • Morphine exerts an immunostimulatory effect on human DCs.
  • Morphine modulates LPS-induced DC maturation and enhances T cell stimulatory capacity.
  • These effects are mediated through opioid receptors and involve p38 MAPK signaling.

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