The effect of leucine-enkephalin (Leu-Enk) on primary humoral immune response was investigated following intracerebroventricular (i.c.v.) administration of the peptide in the rat. Leu-Enk stimulated ...plaque-forming cell (PFC) response in rats i.c.v. injected with 0.1 and 1 μg/kg, whereas doses of 20 and 50 μg/kg exerted immunosuppressive effects. I.c.v. treatment of rats with δ opioid receptor antagonist ICI 174864 and κ opioid receptor antagonist nor-binaltorphimine (
nor-BNI) blocked stimulation and suppression of PFC response induced by Leu-Enk, respectively. The μ opioid receptor antagonist β-funaltrexamine (β-FNA) reversed both immunomodulatory effects produced by Leu-Enk. Since β-FNA alone had no effect on PFC response (unlike ICI 174 864 and
nor-BNI), these data showed that central effects of Leu-Enk on PFC response were mediated by brain μ opioid receptors, and suggested a possible involvement of δ and κ opioid receptors.
Methionine-enkephalin (Met-Enk) induces notable alterations in immune and central nervous system functions. The present study was conducted in order to compare peripheral and central effects of ...Met-Enk on nonspecific immunity, open field behavior and pain perception in the rat. The results showed that 0.2 mg/kg of Met-Enk given intraperitoneally (i.p.) increased concanavalin A (Con-A)-induced paw edema and enhanced basal and phorbol myristate acetate (PMA)-stimulated H(2)O(2) production of peritoneal macrophages. Met-Enk-induced immunopotentiation was antagonized by anti-Met-Enk antibodies (anti-Met-Enk-Ig) and quaternary naltrexone (qNtx). Met-Enk injected i.p. produced an increase of horizontal and vertical locomotor activity in the open field that was reversed by i. p. administration of anti-Met-Enk-Ig and qNtx. The dose of 0.2 mg/kg of Met-Enk applied i.p. did not affect the number of writhes in the test of analgesia. Intracerebroventricular (i.c.v.) injection of Met-Enk, given in a dose that was previously shown to be immunostimulatory, enhanced only basal H(2)O(2) production of peritoneal macrophages, and anti-Met-Enk-Ig antagonized this effect. Besides, i.c.v. treatment with anti-Met-Enk-Ig increased and decreased H(2)O(2) production of peritoneal macrophages under basal and stimulated conditions, respectively. Met-Enk and anti-Met-Enk-Ig injected i.c.v. did not influence activity in the open field and pain sensitivity. Thus, the i.c.v. dose of Met-Enk that was sufficient to modulate immune functions did not influence behavior. It may be concluded that Met-Enk modulated nonspecific immune responses and open field behavior by peripheral mechanisms.
Paper presents one implementation of software solution for processing WebVTT subtitles during playback of HLS streams. Software solution is created by using the functionality of the FFmpeg library. ...Result of using created software solution on HLS streams is creation of overall transport stream, which contains video, audio and subtitle components. In this way successful playback of audio, video and subtitle is enabled.
We have previously demonstrated that central application of leucine–enkephalin (Leu–Enk) elicits potentiation and suppression of humoral immune responses through OP1 (δ) and OP2 (κ) receptors, ...respectively. Interestingly, both effects were found to be additionally dependent on OP3 (μ) receptor function. In the present study, we have further investigated whether opioid receptor interactions underlie the immunomodulatory effects of endogenous opioids as well as exogenously applied methionine–enkephalin (Met–Enk). For that purpose, the plaque-forming cell (PFC) response was determined in rats injected intracerebroventricularly (i.c.v.) with opioid receptor-selective antagonists and Met–Enk. Application of the OP1 antagonist ICI 174864, but not naltrindole, resulted in suppression of the PFC response. In contrast, i.c.v. injection of the OP2 selective antagonist nor-binaltorphimine (nor-BNI) significantly potentiated the PFC response. Both effects, presumably mediated by endogenous opioid peptides, were antagonized by the OP3 receptor antagonist β-funaltrexamine (β-FNA) at a dose that was devoid of immunomodulatory activity. The immunopotentiation of the PFC response induced by Met–Enk was reversed by OP1 receptor antagonists, naltrindole and ICI 174864, but not by β-FNA or nor-BNI.
On the basis of these and previous findings, it may be concluded that central OP3 receptors are permissive for the central immunomodulatory action of endogenous opioid peptides and Leu–Enk. In contrast, the central immunoenhancing effect of Met–Enk appears to be mediated through OP3-independent OP1 receptors.
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