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)

Cells of the immune system produce biologically active adrenocorticotropic hormone (ACTH). Many laboratories, however, have been unable to replicate experiments which demonstrate ACTH in immune cells. Sensitive immunohistochemical staining and digital scanning, confocal microscopy were used to study regulation of ACTH-like immunoreactivity (ACTH-IR) in human mononuclear cells. Cytoplasmic ACTH-IR was induced by corticotrophin releasing factor (CRF)/arginine vasopressin (AVP), and also by protein kinase C (PKC) activation and by the interferon (IFN-alpha beta inducer, Na-polyinosinic-polycytidylic acid (polyIC). Induction of cytoplasmic ACTH-IR was maximal within 6 hr of stimulation with CRF/AVP or phorbol myristate acetate (PMA). Recombinant human interleukin-1 beta (rhIL-1 beta) was also stimulatory, but rhIL-1 alpha had minimal effect. Regulation of ACTH-IR production in immune cells parallels the regulation of ACTH in the anterior pituitary, and ACTH-like material may affect immune responses.
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PMID:Regulation of production of adrenocorticotropin-like proteins in human mononuclear cells. 133 62

Because the immune response appears important in the pathogenesis of MS, anti-inflammatory and immunomodulatory drugs and agents are used as a palliative treatment. Azathioprine alone is minimally efficacious and probably not worth the bother and risk. Cyclophosphamide alone is too toxic. Although cyclosporine A may slow the rate of deterioration in chronic progressive MS, adverse effects may limit its use outside major centers. Gamma interferon provokes exacerbations and should not be used. We do not recommend copolymer-1, alpha or beta interferon, monoclonal antibodies, plasmapheresis, and total lymphoid irradiation except in well-designed experimental protocols. Combination therapy of adrenal cortical steroids (ACS) with other immunosuppressants (cyclophosphamide or cyclosporine) merits further study. We think "pulse" synthetic ACS therapy has advantages over corticotropin and will become the "standard of care" for exacerbations. We also would try it for chronic progression. Even then, with the pulse treatment we still must determine the optimum dose, route, duration, and need for "taper."
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PMID:The peculiar difficulties of therapeutic trials for multiple sclerosis. 169 Aug 38

The levels of met-enkephalin (ME), beta-endorphin (BE), and alpha-interferon (a-IFN) have been determined in the human blood 1 day after dipyridamole administration. Dipyridamole led to an increase in serum a-IFN concentration up to 3 times, and to simultaneous rise of the lymphocytes ability to produce a-IFN. The content of BE did not depend on dipyridamole treatment, but ME level achieved 110 +/- 4.8 pg/ml (compare to 79.5 +/- 7.6 pg/ml in control). Positive interrelation has been found out between individual ME concentrations and lymphocyte abilities to a-IFN production with the coefficient of correlation equal to 0.69. The effect of dipyridamole on ME level is suggested to develop via a-IFN interaction with the opioid systems.
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PMID:[Blood levels of opioid peptides and alpha interferon under the action of dipyridamole]. 214 90

Content of Met-enkephalin in striatum and of beta-endorphin in rat hypophysis were estimated after administration of ethanol and alpha-interferon into the animals. Ethanol decreased Met-enkephalin content in striatum and of beta-endorphin in hypophysis. Preadministration of alpha-interferon into brain ventricles before ethanol administration led to an increase in concentration of Met-enkephalin, while content of beta-endorphin was unaltered. In peripheric administration alpha-interferon normalized content of beta-endorphin in adenohypophysis but did not affect the Met-enkephalin concentration. Effects of alpha-interferon on content of Met-enkephalin and beta-endorphin, related to dissimilar organization of the opiate systems in hypophysis and striatum tissues, are discussed.
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PMID:[Modification by alpha-interferon of ethanol-induced changes in the level of opioid peptides in the rat striatum and hypophysis]. 238 36

Endogenous opioids exert a variety of extra central nervous system (CNS) functions, including modulation of some human lymphocyte functions. The latter opioid activity may result in elevation of human natural killer (NK) function (i.e. by beta-endorphin), which is reversed by an opioid antagonist, Naloxone. Since recent evidence has suggested both structural and functional similarities between lymphokines known to elevate human NK function (interferon and interleukin-2) and endogenous opioids, we investigated if Naloxone could modulate lymphokine-enhanced human NK activity. Naloxone blunted, in a dose-dependent fashion, the NK-enhancing activity of peripheral blood lymphocytes or large granular lymphocytes by recombinant interferon-alpha (IFN-alpha) or interleukin-2 (IL-2). Naloxone decreased the uptake of radiolabelled IL-2 receptors. beta-endorphin also decreased the binding of radiolabelled IL-2 or IL-2 receptor-positive human lymphocytes. Finally, labelled Naloxone was inhibited from binding to phytohaemagglutinin (PHA)-stimulated lymphocytes by either beta-endorphin or IL-2. These findings strongly suggest that human lymphocyte receptors for opioid, IFN or IL-2 molecules, once occupied, have distinct influences on the alternate receptor. In addition, these data further strengthen the potential role of CNS-mediated influences on the human immune system.
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PMID:Interaction between endogenous opioids and IL-2 on PHA-stimulated human lymphocytes. 239 65

Interleukin 2 (IL-2) stimulated the differentiation of human peripheral blood leukocytes into lymphokine-activated killer cells, as well as DNA synthesis of human T lymphocytes. Both effects of IL-2 could be inhibited by prostaglandin E2, a potent stimulator of adenylate cyclase; however, the inhibitory effect of prostaglandin E2 could be overcome by increased concentrations of IL-2. The opposite effects of IL-2 and prostaglandin E2 were paralleled by their respective abilities to inhibit and stimulate cAMP production in intact cells. Other agents, which inhibit adenylate cyclase directly (somatostatin, beta-endorphin, UK 14.3041) or indirectly by activation of protein kinase C (phenylephrine), could stimulate both differentiation and proliferation. None of these agents alone or in combination were as effective as maximal concentrations of IL-2. However, all agents potentiated differentiation and proliferation induced by submaximal and maximal concentrations of IL-2. Additionally, combinations of agents which stimulated protein kinase C with those that inhibited adenylate cyclase were additive in the potentiation of IL-2-induced differentiation. Neither inhibition nor potentiation of IL-2-induced lymphokine-activated killer cell differentiation was accompanied by changes in Tac expression or gamma-interferon production. The data indicate that the stimulation of lymphokine-activated killer cell differentiation and lymphocyte proliferation in human cells share a common initial biochemical signal. Although the inhibition of adenylate cyclase is not sufficient to maximally stimulate either process and cannot bypass the requirement for IL-2, modulation of this enzyme complex, positively or negatively, can regulate the ultimate physiologic response to IL-2.
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PMID:Potentiation of lymphokine-activated killer cell differentiation and lymphocyte proliferation by stimulation of protein kinase C or inhibition of adenylate cyclase. 244 68

On the basis of their properties of noradrenergic and/or thromboxane inhibition, or on their activation of the dopaminergic reward system and/or beta-endorphin, the following substances or treatments are predicted to be effective in treating alcohol or drug addiction: ginger; carbon dioxide; dietary sulfur; methionine; calcium; LHRH; high intensity light; interferon; negative ions; serotonin antagonists such as methysergide and cyproheptadine; guanabenz and guenfacine; antihistamines; head-out water immersion; X-irradiation; and forced unilateral left nostril breathing.
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PMID:Predicting new effective treatments of alcohol addiction on the basis of their properties of inhibition of noradrenergic activity and/or thromboxane or on the activation of the dopamine reward system and/or beta-endorphin. 257 15

Interferon causes profound biological changes when given to patients with cancer and many of these could not be predicted from in vitro or animal model systems. We documented significant changes in hormonal levels for a group of 18 patients who were participants in a Phase I gamma-interferon trial. Adrenocorticotropic hormone, cortisol, and growth hormone were all significantly elevated 2 h after treatment with gamma-interferon, with cortisol and adrenocorticotropic hormone returning to base line by 24 h. A placebo group failed to show this change, suggesting a specific interferon effect. Possible mechanisms for these findings and implications for the use of interferons are discussed.
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PMID:Effects of gamma-interferon on the endocrine system: results from a phase I study. 282 31

We examined the effect of 20 micrograms recombinant gamma-interferon (rec-gamma-IFN) upon corticotropin (ACTH) and cortisol secretion in 10 healthy male controls. We observed that rec-gamma-IFN enhances cortisol secretion with maxima around 3 hours after injection of the test dose. This effect was suppressible by a single dose of 1.5 mg dexamethasone and was not associated with increased ACTH secretion. Rec-gamma-IFN also failed to enhance ACTH secretion from a pituitary cell culture. From these data we conclude that rec-gamma-IFN acts on lymphoid cells which in turn release a yet unidentified substance that directly activates the adrenocortex in a feedback controlled manner.
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PMID:Acute adrenocortical stimulation by recombinant gamma interferon in human controls. 282 52

An increasing amount of data supports the hypothesis that there are bidirectional circuits between the central nervous system (CNS) and the immune system. Soluble products that appear to transmit information from the immune compartment to the CNS include thymosins, lymphokines, and certain complement proteins. Opioid peptides, adrenocorticotropic hormone (ACTH), and thyroid-stimulating hormone (TSH) are additional products of lymphocytes that may function in immunomodulatory neuroendocrine circuits. It is proposed that the term "immunotransmitter" be used to describe molecules that are produced predominantly by cells that comprise the immune system but that transmit specific signals and information to neurons and other cell types. Examples would include thymosin alpha 1 and beta 4, lymphocyte-derived ACTH, TSH, and beta-endorphin, interleukin 1, interferon as well as certain other lymphokines and cytokines. The evidence that certain thymosin peptides can serve as immunotransmitters by modulating the hypothalamic-pituitary-adrenal and gonadal axes will be discussed.
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PMID:Evidence that thymosins and other biologic response modifiers can function as neuroactive immunotransmitters. 286 Dec 35


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