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Morphine directs T cells toward T(H2) differentiation.

S Roy1, S Balasubramanian, S Sumandeep

  • 1Department of Surgery, University of Minnesota, the Minneapolis Veterans Affairs Medical Center, Minneapolis, MN 55417, USA.

Surgery
|August 8, 2001
PubMed
Summary

Morphine use after injury promotes T(H2) cell differentiation via the mu-opioid receptor. This mechanism involves increased IL-4 transcription, partly through NFAT signaling, impacting immune responses.

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Area of Science:

  • Immunology
  • Pharmacology
  • Cell Biology

Background:

  • Cell-mediated immunity failure post-trauma increases morbidity/mortality.
  • This failure may stem from CD4(+) T cells shifting to T(H2) differentiation.
  • Morphine's role in this immune shift is investigated.

Purpose of the Study:

  • To test if morphine after injury promotes T(H2) differentiation via the mu-opioid receptor.
  • To elucidate the molecular mechanisms of morphine-induced T(H2) skewing.

Main Methods:

  • In vitro treatment of human PBMCs and mouse splenocytes with morphine.
  • Cytokine analysis (IL-2, IFN-γ, IL-4, IL-5) using ELISA.
  • Investigation of IL-4 transcription and NFAT binding in response to morphine.

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Main Results:

  • Morphine decreased T(H1) cytokines (IL-2, IFN-γ) and increased T(H2) cytokines (IL-4, IL-5) in wild-type cells.
  • These effects were absent in mu-opioid receptor knockout mice.
  • Morphine enhanced IL-4 mRNA, IL-4 promoter activity, and NFAT binding.

Conclusions:

  • Morphine promotes T(H2) differentiation through mu-opioid receptor signaling.
  • Morphine increases IL-4 transcription, partly via an NFAT-dependent pathway.
  • Findings suggest a mechanism for morphine's impact on immune responses after injury.