MU-opioid receptor-knockout mice: Role of μ-opioid receptor in morphine mediated immune functions

Sabita Roy, Roderick A. Barke, Horace H. Loh

Research output: Contribution to journalArticlepeer-review

131 Scopus citations

Abstract

The role of the μ-opioid receptor in immune function was investigated using μ-opioid receptor knockout mice (MOR-KO). Morphine modulation of several immune functions, including macrophage phagocytosis and macrophage secretion of TNF-α, was not observed in the MOR-KO animals, suggesting that these functions are mediated by the classical μ-opioid receptor. In contrast, morphine reduction of splenic and thymic cell number and mitogen-induced proliferation were unaffected in MOR-KO mice, as was morphine inhibition of IL-1 and IL-6 secretion by macrophages. These latter results are consistent with morphine action on a naloxone insensitive morphine receptor, a conclusion supported by previous studies characterizing a nonopioid morphine binding site on immune cells. Alternatively, morphine may act either directly or indirectly on these cells, by a mechanism mediated by either delta or kappa opioid receptors. Copyright (C) 1998 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)190-194
Number of pages5
JournalMolecular Brain Research
Volume61
Issue number1-2
DOIs
StatePublished - Oct 30 1998

Bibliographical note

Funding Information:
This work was supported by NIH grants DA00564, DA01583, DA05695, K05-DA70554, F. and A. Stark Fund (MMF)-HHL and DA 08188 (SR).

Keywords

  • Knockout
  • Macrophage
  • Morphine
  • T-cells
  • μ-Opioid receptor

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