Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comparative Study
. 1990 May;24(2):141-8.
doi: 10.1016/0165-2478(90)90026-m.

Opioids modulate interleukin-1 production and secretion by bone-marrow macrophages

Affiliations
Comparative Study

Opioids modulate interleukin-1 production and secretion by bone-marrow macrophages

R N Apte et al. Immunol Lett. 1990 May.

Abstract

In the present study, we have assessed the effect of opioids (endorphins, enkephalins and neoendorphins) on production of IL-1 activity by bone-marrow-derived macrophages. None of the neuropeptides induced IL-1 production by itself. However, some of the opioids potentiated IL-1 production and release in macrophages concomitantly stimulated by lipopolysaccharide (LPS) or silica. LPS induced predominantly intracellular IL-1 activity, whereas most of the silica-induced IL-1 was released extracellularly. beta-Endorphin, leucine-enkephalin (leu-enkephalin) and beta-neoendorphin all potentiated both intracellular and extracellular release of IL 1 induced by either LPS or silica. In contrast, alpha-endorphin, methionine-enkephalin (metenkephalin) and alpha-neoendorphin did not influence IL-1 production or release. The potentiating effects of beta-endorphin on LPS-induced IL-1 production/secretion were inhibited by naloxone, pointing to an involvement of opioid receptors.

PubMed Disclaimer

Publication types

LinkOut - more resources