Augmenting effect of opioid peptides on murine macrophage activation

J Neuroimmunol. 1994 Feb;50(1):71-6. doi: 10.1016/0165-5728(94)90216-x.


We investigated the effect of several opioid peptides on the activation of murine peritoneal exudate macrophages (M phi) in vitro. M phi were treated with interferon (IFN) as a priming agent and bacterial lipopolysaccharide (LPS) as a triggering agent in the presence or absence of opioid peptides. M phi activation was assessed by their tumoricidal activity. When treatment with IFN and LPS resulted in a high level activation of M phi, dynorphin-A exerted no further enhancing effect. When treatment induced only weak activation, however, dynorphin-A augmented the M phi activation. Leucine-enkephalin, methionine-enkephalin, and also beta-endorphin had augmenting effects. An opioid receptor antagonist, naloxone, reduced the effect of dynorphin-A and beta-endorphin. When M phi were treated sequentially with IFN and LPS, beta-endorphin operated in combination with LPS only. Moreover, beta-endorphin was effective for already activated M phi. These results indicate that opioid peptides act on M phi via classical opioid receptors, and that responsiveness to opioid peptides is induced in the triggering stage of M phi activation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • Dynorphins / pharmacology
  • Endorphins / pharmacology*
  • Enkephalins / pharmacology
  • Female
  • Macrophage Activation / drug effects*
  • Macrophages / drug effects
  • Macrophages / physiology
  • Mice
  • Mice, Inbred C3H
  • Mice, Inbred C57BL
  • Naloxone / pharmacology
  • beta-Endorphin / pharmacology


  • Endorphins
  • Enkephalins
  • Naloxone
  • beta-Endorphin
  • Dynorphins