Interleukin-6 is differently modulated by central opioid receptor subtypes

Magali Bertolucci, Carlo Perego, Maria Grazia De Simoni

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

The central endogenous opioid system is involved in the modulation of interleukin (IL)-6, an inflammatory cytokine that plays a major role in the acute phase response. The present study evaluates whether specific opioid receptor subtypes are selectively involved in this immnunomodulatory action. IL-1β was administered either intracerebroventricularly or intraperitoneally at the dose of 400 ng to rats pretreated with the μ-antagonist β- funaltrexamine, the δ-antagonist naltrindole, or the κ-antagonist nor- binaltorphimine, each at the doses of 1, 10, and 100 μg/rat intracerebroventricularly. Serum IL-6 levels were measured 2 h later. The results show that μ-receptor blockade increases, whereas δ-receptor blockade decreases IL-6 induction, suggesting that the fine tuning exerted by opioids on the immune system may be achieved through a balance of opposing effects. Moreover the three antagonists affect IL-6 induction by central and peripheral IL-1β with a similar pattern, indicating that the brain endogenous opioid system plays a general role in the regulation of this cytokine.

Original languageEnglish
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume273
Issue number3 42-3
Publication statusPublished - 1997

Fingerprint

Opioid Receptors
Interleukin-6
Opioid Analgesics
naltrindole
Interleukin-1
Cytokines
Acute-Phase Reaction
Immune System
Brain
Serum

Keywords

  • β-funaltrexamine
  • Immunomodulation
  • Interleukin-1
  • Naltrindole
  • Nor- binaltorphimine

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Interleukin-6 is differently modulated by central opioid receptor subtypes. / Bertolucci, Magali; Perego, Carlo; De Simoni, Maria Grazia.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 273, No. 3 42-3, 1997.

Research output: Contribution to journalArticle

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