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It is well documented that endogenous opioid peptides modulate the activity of immune and inflammatory cells. Opioid peptides exert biological effects through at least three opioid receptor types, known as µ, δ and κ. In the present study we have investigated which types of opioid receptors are involved in the opioid peptide-induced modulation of superoxide an/on release from macrophages. Rat peritoneal macrophages were stimulated with zymosan, and treated in vitro with opioid peptides and/or antagonists specific for different opioid receptor types. The results showed that the µ opioid receptor agonist, beta-endorphin, and the k opioid receptor agonist dynorphin A, decreased superoxide anion production. Conversely methionine-enkephalin (Met-Enk) and leucine-enkephalin, that have a preference for δ opioid receptors, did not affect superoxide anion release. Furthermore, we have tested the effect of Met-Enk on superoxide anion release from macrophages under blockade of all receptors with specific antagonists except for one receptor subtype. Accordingly, it was found that the Met-Enk induced increase and decrease of superoxide anion production were mediated through δ1,2 and µκ opioid receptors, respectively. It can be concluded that opposing activity of µ, and κ receptors vs. δ receptors together with the affinity for a ceflain receptor-type determines the effect of a particular endogenous opioid peptide on superoxide anion release from rat peritoneal macrophages

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The effect of opioid peptides on superoxide, anion production in rat peritoneal macrophages stimulated with zymosan: involvement of µ, δ and κ opioid receptors