Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sequential similarities between the tryptophan peptide of myelin basic protein (residues 111-121), luteinizing hormone releasing hormone, melanotropin, adrenocorticotropin (residues 1-13), human leukocyte interferon (residues 28-40), and various segments of human and bovine serum albumin and hen ovalbumin are presented. It is suggested that these structural similarities may explain observations concerning common functional characteristics such as serotonin modulation, immunological activity with the adjuvant muramyl dipeptide, immunological cross-reactivity, and the possible MSH-ACTH-like activity of a pepsin-derived peptide of interferon.
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PMID:'Molecular sandwiches' as a basis for structural and functional similarities for interferons, MSH, ACTH, LHRH, myelin basic protein, and albumins. 620 49

Opioid peptides are present in peripheral blood, and may bind to human lymphocytes. In order to determine their influence on human lymphocytes we studied the effect of endogenous opioid peptides on human lymphocyte natural killer function. Beta-endorphin and several analogues (i.e., gamma-endorphin) are shown to enhance human peripheral blood natural killer function. The enhancement of natural killing by these opioid peptides was dose-dependent and naloxone (an opiate antagonist) reversible. In studying various analogues of beta-endorphin, beta-lipotropin and gamma-endorphin were approximately 3-5 times more effective at enhancing peripheral blood NK function than Leu-enkephalin and -endorphin. In addition, we observed that naloxone reversed human fibroblast interferon mediated enhancement of human blood lymphocyte natural killer function. These observations suggest that circulating endogenous opioid peptides may have a physiologic role in regulating human blood lymphocyte natural killing.
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PMID:Endorphins stimulate normal human peripheral blood lymphocyte natural killer activity. 620 82

We have shown that corticotropin (ACTH), alpha-endorphin, and enkephalins can regulate antibody responses, which suggested a role for neuropeptides in a regulatory circuit between the immune and neuroendocrine systems. ACTH and structurally related peptides were examined here for regulation of mitogen induction of the lymphokine gamma-interferon (IFN gamma) in C57BL/6 mouse spleen cell cultures. Synthetic ACTH1-39 and a porcine pituitary extract containing ACTH activity were potent suppressors of the IFN gamma response. Synthetic ACTH1-39 suppressed the response by approximately 62% at 1 to 3 microM, whereas the porcine extract suppressed by greater than 90% at 1 to 3 microM ACTH. The greater potency of the pituitary extract was shown to be due to the presence of an additional peptide of Mr 2100 that was reactive with antibodies to the N-terminal region of ACTH (ACTH1-13), possessed potent anti-cellular activity against L cells and various transformed cells, but lacked ACTH biologic activity. The anti-cellular peptide suppressed the IFN gamma response by greater than 99% at 0.05 microM. The ACTH1-39 cleavage products, alpha-melanocyte stimulating hormone (alpha MSH; acetylated and amidated ACTH1-13), and corticotropin-like intermediate lobe peptide (CLIP; ACTH18-39) had no effect on IFN gamma production. ACTH1-24, like ACTH1-39, has full steroidogenesis activity but also had no effect on IFN gamma production, which suggests a dissociation of the immunoregulatory and steroidogenic properties of ACTH1-39. ACTH1-39, and possibly also the anti-cellular 2100 Mr peptide, is initially synthesized as the precursor polyprotein pro-opiomelanocortin (POMC). Enzymatic processing of POMC, first to the active ACTH1-39 or the anti-cellular peptide and then to the inactive smaller peptides, probably plays an important role in regulation of lymphokine and antibody production by ACTH and ACTH-related neuropeptides. This is consistent with the recent demonstration of the production of ACTH-like peptides by lymphocytes.
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PMID:Regulation of lymphokine (gamma-interferon) production by corticotropin. 631 43

Sixteen peptides were injected intracerebroventricularly to test their effects on rectal temperature of rabbits in a thermoneutral environment. In initial tests 5 micrograms alpha-MSH, ACTH(1--24), oxytocin, vasopressin and glucagon altered body temperature while ACTH(1--10), cholecystokinin, contraceptive tetrapeptide, gastrin, insulin, interferon, leupeptin, LHRH, panhibin (somatostatin), and proctolin did not. Bombesin also altered body temperature but in no consistent direction. In further tests on the effective peptides 1.25--5.0 micrograms alpha-MSH and ACTH(1--24) produced dose-related decreases in rectal temperature as great as 1.0 degrees C. The same doses of oxytocin and glucagon produced small, prolonged hyperthermias which did not exceed 0.4 degrees C. Vasopressin caused rapid development of small increases in rectal temperature; temperature returned to normal in 2--3 hr. The results suggest that five of the peptides tested may have roles in central mediation of normal body temperature, hypothermia, hyperthermia and fever.
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PMID:Central administration of peptides alters thermoregulation in the rabbit. 724 7

The neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) is known to suppress cytokine-mediated inflammation. In addition, we previously found that alpha-MSH suppressed the production of the proinflammatory cytokine interferon (IFN)-gamma by antigen-stimulated primed lymph node T cells. This immunosuppressive activity of alpha-MSH on lymph node T cell cultures is similar to that of interleukin (IL)-4. To further examine the potential 'IL-4 like' activities of alpha-MSH, antigen-stimulated lymph node T cell cultures were treated with alpha-MSH in the presence of neutralizing anti-IL-4 antibodies. The enhanced production of IFN-gamma caused by the presence of anti-IL-4 alone in the T cell cultures was squelched by alpha-MSH. This demonstrated that in these cultures, alpha-MSH regulation of IFN-gamma production operates in a fashion similar to that of endogenous IL-4. Addition of exogenous IL-4 to antigen-stimulated lymph node T cell cultures did not intensify alpha-MSH down-regulation of IFN-gamma production, and the addition of alpha-MSH to IL-4-treated cultures did not further depress IFN-gamma production. These and the previous results suggest that the mechanism of alpha-MSH suppression of IFN-gamma production in the antigen-stimulated T cell cultures is similar to, but independent of, IL-4. When antigen-presenting cells (APCs) were the only cells in the antigen-stimulated T cell cultures treated with alpha-MSH, there was a significant reduction (60-70%) of APC elicitation of IFN-gamma production by untreated primed T cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alpha-melanocyte-stimulating hormone suppresses antigen-stimulated T cell production of gamma-interferon. 748 33

We investigated the effect of several opioid peptides on the activation of murine peritoneal exudate macrophages (M phi) in vitro. M phi were treated with interferon (IFN) as a priming agent and bacterial lipopolysaccharide (LPS) as a triggering agent in the presence or absence of opioid peptides. M phi activation was assessed by their tumoricidal activity. When treatment with IFN and LPS resulted in a high level activation of M phi, dynorphin-A exerted no further enhancing effect. When treatment induced only weak activation, however, dynorphin-A augmented the M phi activation. Leucine-enkephalin, methionine-enkephalin, and also beta-endorphin had augmenting effects. An opioid receptor antagonist, naloxone, reduced the effect of dynorphin-A and beta-endorphin. When M phi were treated sequentially with IFN and LPS, beta-endorphin operated in combination with LPS only. Moreover, beta-endorphin was effective for already activated M phi. These results indicate that opioid peptides act on M phi via classical opioid receptors, and that responsiveness to opioid peptides is induced in the triggering stage of M phi activation.
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PMID:Augmenting effect of opioid peptides on murine macrophage activation. 790 88

This study determined the effects of neuropeptides and neuroendocrine hormones at the cellular level of the immune response using a murine macrophage cell line, J774, which exhibits a chemiluminescent oxidative burst upon acute stimulation with zymosan. We report that the zymosan-triggered oxidative burst of J774 cells can be modulated by the opioid peptides beta-endorphin (beta-END) and dynorphin A (DYN) in a naloxone-reversible fashion. Norepinephrine (NE) also modulated chemiluminescence (CL) emission of J774 cells, with dose-dependent suppression of CL dependent upon co-incubation with gamma-interferon (gamma-INF). Without gamma-INF co-incubation, NE shared with the opioid peptides beta-END and DYN the ability to modulate oxidative burst, producing an inverted-U dose response. These data indicate that J774 cells may be useful for explaining some mechanisms through which the neuroendocrine system interacts with the immune system.
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PMID:Modulation of chemiluminescence in a murine macrophage cell line by neuroendocrine hormones. 810 66

In in vivo studies, a conditioned increase in NK cell activity can be obtained by pairing odor of camphor (conditioned stimulus, CS) with poly I:C (unconditioned stimulus, US) in a single-association paradigm. We identified interferon (IFN) as the signal that reaches the central nervous system (CNS) to make an association with the camphor CS. We have also established that the CS/US association is an IFN-dependent step, and the expression stage is an opioid-dependent pathway which can be blocked with naltrexone and dexamethasone. Here we have focused on the signals responsible for the expression of conditioned augmentation of natural killer (NK) cell activity. The possible efferent signal molecules that were considered were IFN, beta-endorphin (beta-END), and adrenocorticotropic hormone (ACTH). Plasma levels of beta-END and ACTH of conditioned and control mice were quantitated by radioimmunoassay, and the changes in IFN message in the spleen cells were determined by Northern hybridization analysis. Results indicate that the ACTH levels and IFN-alpha gene expression were higher in the conditioned animals than in the controls. These studies support the view that ACTH released from the pituitary gland is involved in the up-regulation of IFN-alpha, which in turn stimulates the NK cells in the spleen.
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PMID:Efferent signal(s) responsible for the conditioned augmentation of natural killer cell activity. 852 88

Recent studies indicate the production of adrenocorticotropic hormone (ACTH) by human mononuclear leucocytes constitutively or in response to hypothalamic factors and interferon inducers. These results have led to the proposal that the control mechanisms for the proopiomelanocortin (POMC) gene in lymphocytes may be similar to that of pituitary cells. After chronic ethanol treatment, changes in the pituitary POMC mRNA in rats have been reported, but so far nothing is known about changes in the POMC gene expression in lymphocytes under these conditions. Therefore, the expression of the POMC gene was investigated in human peripheral lymphocytes in both volunteers and alcoholics. POMC mRNA levels in these cells were significantly increased in alcoholics, with one alcoholic showing an even more than five times higher POMC mRNA level compared to the other patients. After detoxification, a significant decrease in the POMC mRNA of alcoholic patients was observed, except in the one with the extremely elevated POMC mRNA level, where the opposite occurred. An influence of chronic ethanol ingestion on POMC gene expression in lymphocytes could be assumed. The observed changes seem to be correlated with ethanol intake, because the elevated POMC mRNA amounts found in lymphocytes of alcoholics after admission to the hospital were already declining after the detoxification period.
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PMID:Quantification of proopiomelanocortin mRNA in peripheral lymphocytes of alcoholics. 942 36

1. Alveolar rabbit macrophages were studied for superoxide and nitric oxide production at basal levels and upon stimulation with phorbol myristate acetate (PMA), zymosan, cytokines (two types of interferon), and lipopolysaccharide in the presence (or absence) of beta-endorphin or hydroxylamine or both. 2. Beta-endorphin diminished (statistically significant at concentration of 10(-8) M) superoxide production by PMA-stimulated macrophages but augmented reactive oxygen generation (10(-12) M beta-endorphin) by zymosan-activated cells. 3. In the presence of hydroxylamine, beta-endorphin had a visible (albeit not statistically significant) suppressive effect on nitrite production by PMA-activated cells. 4. Cytokine-stimulated macrophages enhanced nitric oxide production in the presence of hydroxylamine and beta-endorphin in culture supernatants. 5. Beta-endorphin exerted different modulatory effects on the production of reactive oxygen and nitrite intermediates by rabbit alveolar macrophages (suppression or enhancement) that was strictly dependent on the method of cell activation.
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PMID:Influence of beta-endorphin on the production of reactive oxygen and nitrogen intermediates by rabbit alveolar macrophages. 970 7


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