Abstract
The role of the neuropeptide beta-endorphin on interleukin 1 (IL-1) production by murine bone marrow-derived macrophages was assessed. Beta-endorphin by itself did not induce IL-1 generation. However, over a wide range of concentrations (10(-6)-10(-14) M) beta-endorphin potentiated lipopolysaccharide (LPS)- or silica-induced production of intracellular and extracellular IL-1. This enhancement by beta-endorphin was most evident when using suboptimal doses of LPS. Naloxone, a competitive inhibitor of beta-endorphin opioid receptor interactions, abrogated the enhancing effects of beta-endorphin on LPS-induced IL-1 production. Furthermore, LPS-induced IL-1 production by macrophages (in the absence of added beta-endorphin) was also partially inhibited following treatment with naloxone, suggesting that opioids derived from activated macrophages may also modulate IL-1 generation and secretion. Thus, beta-endorphin-opioid receptor interactions result in enhanced production of immunomodulators such as IL-1.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
