Dynorphin A enhances mitogen-induced proliferative response and interleukin-2 production of rat splenocytes

Neuropeptides. 1999 Apr;33(2):137-43. doi: 10.1054/npep.1999.0008.

Abstract

It has been well known that immune function is modulated by endogenous opioid peptides: beta-endorphin and enkephalins. However, the effect of dynorphin A on the immune function has not been well documented. In this study, we investigated dynorphin A in the regulation of mitogen-induced proliferation and and interleukin-2 (IL-2) production of rat splenocytes. The results showed that dynorphin A 1-13 as well as dynorphin A 1-17 enhanced concanavalin A-stimulated [(3)H] thymidine uptake 46-112% and IL-2 production in a dose-dependent fashion. These effects were reversed by naloxone and norBNI, a selective kappa-receptor antagonist. Dynorphin A reduced cyclic AMP contents in spenocytes in naloxone and norBNI reversible fashion. The data suggest that dynorphin A enhanced mitogen-stumulated lymphocyte proliferation and IL-2 production via kappa-opioid receptor and cAMP pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analgesics, Opioid / pharmacology
  • Animals
  • Cells, Cultured
  • Concanavalin A / pharmacology*
  • Dynorphins / pharmacology*
  • Interleukin-2 / biosynthesis*
  • Lymphocyte Activation / drug effects*
  • Lymphocytes / drug effects
  • Lymphocytes / immunology*
  • Male
  • Naloxone / pharmacology
  • Naltrexone / analogs & derivatives
  • Naltrexone / pharmacology
  • Narcotic Antagonists / pharmacology
  • Peptide Fragments / pharmacology
  • Rats
  • Rats, Sprague-Dawley
  • Spleen / immunology

Substances

  • Analgesics, Opioid
  • Interleukin-2
  • Narcotic Antagonists
  • Peptide Fragments
  • Concanavalin A
  • Naloxone
  • norbinaltorphimine
  • Naltrexone
  • dynorphin (1-13)
  • Dynorphins