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)

During long-term interferon alpha-2b (IFN) therapy of Philadelphia chromosome-positive chronic myelogenous leukemia (CML) patients, short-term effects of tumor necrosis factor alpha (TNF) on peripheral leukocyte counts, as well as cortisol and corticotropin (ACTH) release were studied. TNF (40-160 micrograms/m2) was given as a 2-h infusion on 5 consecutive days every 3 weeks, in addition to s.c. daily IFN injections (4 mio U/m2), to four (two male/two female) patients, who had been treated for more than 8 months with IFN and additionally for 0-7 months with TNF. Leukocyte counts, cortisol, and ACTH were determined at 30-min intervals between 4 p.m. and midnight. Profiles were determined the day before and on day 1 of TNF therapy. Leukocyte numbers decreased 30 min after start of TNF administration and increased 30-60 min later with a rebound until the next TNF application. The increase of leukocyte counts was due mostly to neutrophil granulocytes. ACTH levels increased 30 min, cortisol 60 min, and leukocyte counts 90 min after start of TNF infusion. Metopirone, an inhibitor of cortisol synthesis given to one patient, suppressed the TNF-induced stimulation of cortisol secretion and subsequent increase of leukocyte counts, while ACTH blood levels were enhanced. It was concluded that leukocyte count increases after TNF/IFN administration might be related to TNF-evoked cortisol secretion.
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PMID:Relation between leukocyte counts and cortisol secretion in CML patients undergoing combined TNF alpha/IFN alpha therapy. 132 78

Interleukin-1 (IL-1) and interferon alpha (IFN alpha), cytokines originally detected in immunological cells, now have been shown to produce nonimmunological host defense responses of central and peripheral origins. These cytokines are released from glial cells in the brain in pathological states. Local application of IL-1 beta and IFN alpha to thermosensitive neurons in the preoptic and anterior hypothalamus and glucose responsive neurons in the ventromedial hypothalamus in vivo and in vitro, altered the activity in appropriate ways to explain the cytokines-induced fever and anorexia, respectively. The responses to IL-1 beta, but not to IFN alpha, were blocked by sodium salicylate, suggesting the involvement of synthesis of prostaglandins. alpha MSH, an endogenous antipyretic and a possible antagonist of IL-1 beta at lymphocytes, specifically depressed the responses to IL-1 beta, but not those to IFN alpha. In contrast, the action of IFN alpha was reversibly blocked by naloxone, suggesting the opioid receptor mediation. Intracerebral injection of IFN alpha and beta-endorphin in the rat and mouse resulted in the suppression of cytotoxic activity of natural killer cells in the spleen by activation of brain opioid receptor, which was shown to be mediated predominantly by splenic sympathetic nerves. The results suggest a view that immune cytokines may provide afferent links for the regulatory circuits between the brain and the immune system.
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PMID:Immune cytokines and regulation of body temperature, food intake and cellular immunity. 195 24

Treatment of lymphocytes with inducers of interferon alpha (IFN-alpha) results in the production of corticotropin (ACTH) and endorphin-like activities. The pro-opiomelanocortin-derived hormones ACTH and alpha-, beta-, and gamma-endorphin and the structurally related hormones [Leu]- and [Met]enkephalin were therefore tested for their effects on the in vitro antibody response of mouse spleen cells. ACTH and alpha-endorphin were potent inhibitors (>/=80% suppression) of the antibody response to the T-cell-dependent antigen sheep erythrocytes at a concentration of 0.5 muM. [Met]- and [Leu]enkephalin were moderate inhibitors (approximately 60% suppression) at 0.2-2 muM, and beta- and gamma-endorphin were minimal inhibitors (approximately 20% suppression) at 5-6 muM. At higher concentrations ACTH also inhibited the antibody response to the T-cell-independent antigen dinitrophenyl-Ficoll, suggesting that T-cell function was more sensitive to blockage by these hormones than was B-cell function. ACTH and IFN had similar suppression properties; thus, the hormone-like activities associated with IFN-alpha may play a role in IFN-induced immunosuppression. alpha-Endorphin immunosuppression was blocked by naloxone, which suggested that alpha-endorphin exerted its effects through binding to opiate-like receptors on the spleen cells. The failure of beta-endorphin to suppress the immune response significantly was not due to its failure to bind to the opiate-like receptors because it blocked alpha-endorphin-induced suppression. Direct evidence for both opiate and ACTH receptors on the spleen cells was obtained in binding studies with labeled enkephalin and ACTH. Such studies revealed the presence of both high- and low-affinity receptors. The data show that neuroendocrine polypeptide hormones can regulate the immune response.
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PMID:Regulation of the in vitro antibody response by neuroendocrine hormones. 628 70

Alterations of the hypothalamic-pituitary-adrenal (HPA) axis are common in HIV infection. To characterize further the site of these derangements and their possible causes, eight male drug addicts with symptomatic HIV infection (stage IV C2) underwent the following investigations: repeated baseline determinations of cortisol, adrenocorticotropin (ACTH), interleukin 1 beta (IL-1 beta), IL-6 and interferon alpha (IFN-alpha); and ovine corticotropin-releasing hormone (CRH) test (100 micrograms IV) for ACTH and cortisol determinations. Baseline cortisol levels were either normal or elevated in all patients. A significant linear correlation was found between baseline levels of cortisol and both IL-6 (r = 0.955; p < 0.001) and IL-1 beta (r = 0.863; p < 0.005), but not between cortisol and ACTH or between ACTH and circulating cytokines. Both ACTH and cortisol responses to CRH were nearly absent in six out of eight patients, and delayed in the others. The areas under the curves of both ACTH and cortisol after CRH were significantly lower in HIV patients than in a group of eight healthy control subjects (p = 0.0157 for ACTH and p = 0.046 for cortisol). Out data suggest the possibility of an inappropriate stimulation of the HPA axis in symptomatic HIV infection by HIV-induced release of cytokines, with a blunted pituitary and adrenal response to CRH.
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PMID:Altered adrenocorticotropin and cortisol response to corticotropin-releasing hormone in HIV-1 infection. 765 41

Our findings reviewed in this article have revealed that the stimulation of opioid receptors of the hypothalamic neurons by interferon alpha and beta-endorphin synthesized in the brain or by stress causing the opioid-dependent analgesia suppresses the natural killer cytotoxicity, an important component of immunosurveillance, through an activation of the hypothalamic CRF-sympathetic nervous system.
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PMID:The hypothalamo-sympathetic nervous system modulates peripheral cellular immunity. 869 99