Regulation of interleukin-1β and interleukin-8 production by agonists of μ and δ opiate receptors in vitro

Abstract

The studies reported here showed that beta-endorphin at concentrations of 10(-7)-10(-11) M increased interleukin-1beta (IL-1beta) production in unfractionated leukocyte suspensions both in the presence of 0.1 microg/ml lipopolysaccharide (LPS) and in cultures not stimulated with LPS. Interleukin-8 (IL-8) production by leukocytes was inhibited by beta-endorphin at concentrations of 10(-7) and 10(-11) M in the presence of LPS. The stimulatory effect of beta-endorphin on IL-1beta production was not blocked by naloxone or naltrindole. Suppression of IL-8 production was blocked by naloxone and naltrindole. In the mononuclear cell and neutrophil fractions, beta-endorphin and the delta agonist DADLE increased IL-1beta synthesis in both the spontaneous and stimulated versions of the test, while beta-endorphin and the delta agonist DADLE inhibited IL-8 production in the mononuclear cell and neutrophil fractions only in LPS-stimulated cultures. The mu agonist DAGO had no effect on IL-1beta production by mononuclear cells or neutrophils, though it suppressed LPS-induced secretion of IL-8 by neutrophils.

Effects of β-endorphin on the production of reactive oxygen species, IL-1β, Tnf-Α, and IL-10 by murine peritoneal macrophages in vivo

“…Earlier, we have demonstrated [7] that, in vitro, β-endorphin enhances the production of IL-1β in human peripheral blood leukocyte cultures stimulated with lipopolysaccharide. In mice deficient for β-endorphin, an increase in the levels of IL-6 and TNF-α was observed in response to stimulation with lipopolysaccharide [12].…”

“…We have previously demonstrated [7] that β-endorphin suppresses the secretion of TNF-α and stimulates the production of IL-1β by the human peripheral blood leukocytes, as well as decreases the levels of IL-8 in granulocyte cultures in vitro. We have also revealed [8] that reactive oxygen species (ROS) production by human peripheral blood leukocytes is significantly decreased in vitro under the action of β-endorphin.…”

Effect of Dynorphin A (1-17) on Proliferation and IL-2, IL-4, IFN-γ Production by Peripheral Blood Mononuclears

“…The stimulatory effect of β-endorphin on the lymphocyte proliferative response is amplifi ed in the presence of naloxone and the intensity of this effect depended on naloxone concentration [1]. Stimulation of IL-1β production in the presence of β-endorphin was not abolished by naloxone and was amplifi ed by δ-antagonist naltrindole [8]. Hence, the presence of certain concentrations of the agonist and antagonist in the culture in some cases leads not to discontinuation, but to amplifi cation of the fi nal effect.…”

“…The structure of prodynorphin includes amino acid sequences of α-and β-neoendorphins, dynorphin A (1-17), and dynorphin B (rimorphin) [3]. Prodynorphin processing can result in the formation of shorter dynorphin A fragments, for example (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13) and (1)(2)(3)(4)(5)(6)(7)(8). The dynorphin group peptides regulate generalized and local neurogenic processes, digestion, reproduction, lactation, development of the common adaptation syndrome, and congenital and acquired immunity reactions [7].…”

Effect of opioid peptides on oxygen-dependent microbicidal activity of peripheral blood neutrophils

“…In our opinion, this phe nomenon is directly connected with intercellular interaction processes. In the leukocyte suspension, opioids stimulate the in vitro production of IL 1β, an important proinflammatory factor markedly activat ing the functional activity of granulocytes, by leuko cytes [14]. At the same time, the is no production of IL 1β by purified monocytes in the presence of β endorphin [15].…”