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

It has been demonstrated that ß-endorphin stimulates the zymosan-induced secretion of reactive oxygen species and suppresses the spontaneous production of IL-1ß and IL-10 by murine peritoneal macrophages in vivo.

Effects of ß-endorphin on functional activity of mouse splenocytes under conditions of in vivo blockade of µ,δ-opioid receptors.

Blockade of δ-receptors with naltrindole under conditions of systemic immunization abolished the stimulatory effect of ß-endorphin (0.0005 µg/kg) on the counts of antibody-producing cells and the titer of antierythrocyte antibodies. Injection of ß-endorphin to mice led to stimulation of concanavalin A-induced proliferative activity of splenocytes and IL-4 secretion by the naloxone-dependent mechanism. The peptide did not modify the production of IL-2 and IFN-γ.

Effect of glycolipid Rhodococcus biosurfactant on secretory activity of neutrophils in vitro.

Glycolipid biosurfactant synthesized by nonpathogenic strain Rhodococcus ruber IEGM231 modulated the production of ROS and IL-8 by peripheral blood neutrophils in spontaneous and stimulated cultures. Secretion of IL-1ß Ð¸ TNF-α by neutrophils in the presence of biosurfactant changed insignificantly.

ß-Endorphin effects on antibody production, proliferation, and secretion of Th1/Th2 cytokines in vivo.

Intraperitoneal injection of ß-endorphin in doses of 1, 0.01, and 0.0005 µg/kg under conditions of systemic immunization increased the count of antibody-producing cells in the spleen and the titer of anti-erythrocyte antibodies in the plasma of experimental animals. Intraperitoneal ß-endorphin stimulated proliferative activity of splenocytes in mice in the presence of both B- and T-cell mitogen, did not change the production of IFN-γ, reduced the level of IL-2, and stimulated the secretion of IL-4, the main Th2-polarizing factor.

Endogenous opioid peptides in regulation of innate immunity cell functions.

Endogenous opioid peptides comprise a group of bioregulatory factors involved in regulation of functional activity of various physiological systems of an organism. One of most important functions of endogenous opioids is their involvement in the interaction between cells of the nervous and immune systems. Summary data on the effects of opioid peptides on regulation of functions of innate immunity cells are presented.

Modulation of cytokine secretion and oxidative metabolism of innate immune effectors by Rhodococcus biosurfactant.

The glycolipid biosurfactant complex from Rhodococcus ruber IEGM 231 had a stimulatory effect on the production of IL-12, IL-18, and reactive oxygen species by cells of the innate immunity. This effect depended on the composition of cell cultures and presence of LPS. It was primarily observed in non-stimulated cultures. The glycolipid biosurfactant complex had little effect on IL-10 secretion by monocytes and mononuclear cells.

In vitro immunomodulating activity of biosurfactant glycolipid complex from Rhodococcus ruber.

The biosurfactant glycolipid complex synthesized by Rhodococcus ruber actinobacteria is not toxic and exhibits no appreciable effect on proliferative activity of peripheral blood leukocytes. In the monocyte fraction, the biosurfactant activates the production of IL-1beta and TNF-alpha cytokines without modifying the production of IL-6. In the mononuclear fraction, the glycolipid biosurfactant exhibited no effects on the production of IL-1beta, TNF-alpha, and IL-6. These results indicate good prospects for further studies of immunomodulating and antitumor activities of biosurfactant drug.

Effect of beta-endorphin on production of antibodies and IL-4 under conditions of opioid receptor blockade.

beta-Endorphin in vivo produced different effects on antibody production depending on the administered dose. Blockade of opioid receptors with naloxone (but not naltrindole) abolished the effects of beta-endorphin. The peptide activated IL-4 production in vitro via activation of delta-opioid receptors.