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Opioids modulate interleukin-1 production and secretion by bone-marrow macrophages
R N Apte1, S K Durum, J J Oppenheim
1Biological Carcinogenesis Development Program Resources, Inc.
Immunology Letters
|May 1, 1990
Summary
Certain opioids enhance interleukin-1 (IL-1) production by macrophages when stimulated. Beta-endorphin and related compounds potentiate IL-1 release, suggesting a role for opioid receptors in immune responses.
Area of Science:
- Immunology
- Neuroendocrinology
- Cell Biology
Background:
- Opioids, including endorphins, enkephalins, and neoendorphins, are known for their roles in pain modulation and mood regulation.
- Interleukin-1 (IL-1) is a key cytokine involved in inflammatory and immune responses.
- Macrophages are critical immune cells that produce and release various cytokines, including IL-1.
Purpose of the Study:
- To investigate the effects of different opioid neuropeptides on the production and release of IL-1 activity by bone-marrow-derived macrophages.
- To determine if opioids can modulate IL-1 production independently or in conjunction with immune stimuli like lipopolysaccharide (LPS) or silica.
Main Methods:
- Bone-marrow-derived macrophages were cultured and treated with various opioid neuropeptides (endorphins, enkephalins, neoendorphins).
- Macrophages were stimulated with lipopolysaccharide (LPS) or silica, with or without opioid treatment.
- Interleukin-1 (IL-1) activity was measured, distinguishing between intracellular and extracellular levels.
- The effect of naloxone, an opioid receptor antagonist, was assessed on opioid-potentiated IL-1 production.
Main Results:
- None of the tested neuropeptides induced IL-1 production on their own.
- Beta-endorphin, leucine-enkephalin, and beta-neoendorphin significantly potentiated IL-1 production and release when macrophages were stimulated by LPS or silica.
- LPS primarily induced intracellular IL-1, while silica induced predominantly extracellular IL-1 release.
- Alpha-endorphin, methionine-enkephalin, and alpha-neoendorphin did not affect IL-1 production or release.
- The potentiating effect of beta-endorphin on LPS-induced IL-1 was reversed by naloxone, indicating opioid receptor involvement.
Conclusions:
- Specific opioids, notably beta-endorphin, leucine-enkephalin, and beta-neoendorphin, can modulate IL-1 production in macrophages.
- These opioids enhance IL-1 release in response to immune stimuli like LPS and silica, suggesting a cross-talk between the opioid and immune systems.
- The findings highlight the involvement of opioid receptors in regulating cytokine production by macrophages and offer insights into neuro-immune interactions.