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)

In concert with the known effects of stress on immune function, we examined a possible neurohumoral connection. The endogenous opiates beta-endorphin, dynorphin, and methionine-enkephalin were assessed for their in vitro effects on human natural killer cell activity, antigen-specific cytolysis, and numbers and ratios of T cells and T-cell subsets. Preincubation with beta-endorphin, an opiate released into the circulation during various stresses, caused a 50% reduction in natural killer cell activity. All endogenous opiates significantly decreased antigen-specific cytolysis. Inhibition of cytolysis in vitro was not mediated through an alteration of T-cell subsets or inhibition of T-cell soluble factors (interleukin 2). The direct effects of these opiates on cytolytic T-cell and natural killer cell function may provide a link between stress and disease susceptibility.
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PMID:The in vitro effects of endogenous opiates on natural killer cells, antigen-specific cytolytic T cells, and T-cell subsets. 348 36

Three experiments were performed to determine the effect of stress on the neuroendocrine-immune system in nonhuman primates. In Experiment 1 the diurnal variation in cell and hormone levels was determined. The percentages of neutrophils, monocytes, and eosinophils fluctuated throughout the 24-hr period, while white blood cell (WBC), neutrophil-to-lymphocyte ratio (N:L), hemoglobin (Hgb), natural killer cell cytotoxicity (NK activity) and beta-endorphin levels did not. Experiment 2 investigated the effects of ketamine and restraint on behavior. Scratching was increased in control monkeys and animals receiving ketamine, whereas passivity was increased in chair-restrained animals. In Experiment 3, eight adult male rhesus monkeys were restrained in primate chairs at 0600h. Behavior was filmed for 3 hr and blood samples were collected at 0700, 0800, and 0900. Whole blood was analyzed for total WBC and percentage of each leukocyte type. NK activity was also measured. Plasma levels of cortisol and beta-endorphin were determined and behavior was quantitated from video-records. WBC and the percentage of neutrophils increased during the restraint period, while the percent lymphocytes and monocytes decreased. NK activity also decreased over time after restraint whereas plasma cortisol and beta-endorphin levels increased significantly. Although after the 3 hr of restraint stress, changes were found in hormone levels, behavior, and NK activity, there were no significant correlations between the parameters measured. Thus, our results indicate that there is not a common neuroendocrine response or single neuroendocrine mediator that results in predictable behavioral changes and immune suppression following stress.
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PMID:Consequences of restraint stress on natural killer cell activity, behavior, and hormone levels in rhesus macaques (Macaca mulatta). 841 48

To examine the potential role of stress hormones in the progression of HIV infections, we developed an in vitro model system that investigates the effects of cortisol, adrenocorticotropin-releasing hormone (ACTH) and beta-endorphin on the natural killer cell activity of lymphocytes from normal subjects and AIDS patients. The system employs a 4 hr 51Cr release assay and K562 target cells. Direct addition of cortisol (0.05, 0.1, and 0.2 microgram/ml) or ACTH (10(-6) to 10(-8) M) to the mixture of effector and prelabeled target cells did not produce any significant immunoregulatory effects on the NK cell activity of normal lymphocytes. Direct addition of beta-endorphin (10(-13) to 10(-17) M) to the mixture of effector and prelabeled target cells did not produce any significant immunoregulatory effects on the NK cell activity of lymphocytes from normal or AIDS subjects. However, cortisol and ACTH significantly inhibited the NK activity of lymphocytes from AIDS patients. The selective inhibitory effects of cortisol and ACTH in patients with HIV infections are consistent with a model which proposes that stress related neurohormones and/or neuropeptides may be involved in the progression of HIV infections.
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PMID:Selective inhibitory effects of stress hormones on natural killer (NK) cell activity of lymphocytes from AIDS patients. 854 34

Research from our laboratory has demonstrated that the presentation of an aversive conditioned stimulus produces pronounced suppression of several in vitro measures of immune status. The present study was designed to evaluate the role of central corticotropin-releasing hormone (CRH) in the mechanisms mediating these conditioned effects. The aversive conditioned stimulus was a distinct environment that had previously been associated with electric footshock. Lewis rats received intraventricular administration of either buffered saline or a dose of the CRH-selective receptor antagonist alpha-helical CRH(9-41) (0, 0.5, 5, or 50 micrograms) prior to exposure to the aversive conditioned stimulus or home cage control treatment. The aversive conditioned stimulus produced decreases in splenic natural killer cell activity, splenocyte responsiveness to the mitogens concanavalin A (ConA), phytohemagglutinin (PHA), lipopolysaccharide (LPS), and the combination of ionomycin and phorbol myristate acetate (PMA), blood leukocyte responsiveness to ConA and PHA, and the production of interleukin-2 and interferon-gamma by activated splenocytes. The conditioned stimulus also produced an increase in plasma levels of corticosterone. Pretreatment with alpha-helical CRH(9-14) completely blocked the conditioned stimulus-induced suppression of natural killer cell activity. The CRH antagonist had no attenuative effect on the conditioned suppression of splenocyte or blood leukocyte proliferation in response to mitogens, or the production of interleukin-2 or interferon-gamma by activated splenocytes. There was also no effect of alpha-helical CRH(9-14) on the conditioned stimulus-induced increase in plasma corticosterone. These findings suggest that conditioned stimulus-induced suppression of natural killer cell activity is mediated by a mechanism that involves activity at central CRH receptors, and that this conditioned modulation is independent of HPA activation. Furthermore, these results indicate that the mechanisms involved in conditioned stimulus-induced suppression of proliferative or cytokine production responses are distinct from those involved in the modulation of natural killer cell activity.
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PMID:Corticotropin-releasing hormone is involved in conditioned stimulus-induced reduction of natural killer cell activity but not in conditioned alterations in cytokine production or proliferation responses. 855 20

The aims of the two studies were to investigate the relationship between emotions and immune responses in an experimental setting by inducing social fear and to broaden our understanding of bodily reactions by examining both cardiovascular and hormonal responses. Seventy-nine healthy subjects were confronted with a situation in which relatively strong social fear was induced in the laboratory. Social fear was induced by having to prepare and give an oral presentation in front of an audience. Thirty additional healthy subjects formed a control group; they followed exactly the same procedure, but, instead of the "public speaking situation," they were subjected to a nondemanding task of the same duration. The results indicate that public speaking evoked fear as shown by both elevated feelings of tenseness and negative bodily sensations. Moreover, the data clearly show enhanced cardiovascular activity, elevated plasma hormone levels, and changes in immunological parameters (natural killer cell number and T helper/inducer cells). The control group reported significantly less feelings of tenseness and negative bodily sensations and showed a decrease in cortisol, prolactin, and beta-endorphin levels. Although some variation on immune responses was present, no variation on cardiovascular activity occurred in the control group during the experiment. The results show that there is indeed a relationship between emotion and immune responses. In addition, the data collected on body responses point to a direct mediating effect of sympathetic-adrenal medulla activity and an indirect mediating effect of hypothalamo-pituitary-adrenal axis activity.
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PMID:Experimental social fear: immunological, hormonal, and autonomic concomitants. 877 27

The immune system and the neuroendocrine system are closely interconnected having such means of bidirectional communication and regulation. In this review, a hypothesis is put forward regarding the possible role of beta-endorphins in the pathogenesis of autoimmune diseases: It is suggested that the increased cytokine production in immunoinflammatory disorders induces production of beta-endorphins from the pituitary and the lymphocytes; the enhanced level of beta-endorphin causes inhibition of human T helper cell function, which potentially down-regulate the antibody production. Also the beta-endorphin-induced enhancement of the natural killer cell activity may suppress the B cell function. In addition, beta-endorphin also exerts a direct inhibitory effect on the antibody production. Thus, in autoimmune disorders the enhanced cytokine level may via stimulation of the production of beta-endorphins exert a negative feed back on the antibody production and potentially so on the production of autoantibodies.
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PMID:Beta-endorphin and the immune system--possible role in autoimmune diseases. 882 74

The effect of [Met5]enkephalin, [Leu5]enkephalin, proenkephalin, dynorphin-(1-17) or beta-endorphin on the cytotoxic (51Cr release assay) activity of natural killer cells and macrophages/monocytes was studied in mice. It was found that a single i.p. injection of [Met5]enkephalin, [Leu5]enkephalin, beta-endorphin, dynorphin or proenkephalin as well as repeated treatment with both enkephalins increased natural killer cell activity. In vitro only [Met5]enkephalin stimulated natural killer cells. Opioid peptides did not affect the cytotoxic activity of macrophages/monocytes. In addition to functional alterations, both enkephalins and beta-endorphin increased the percentage of cells with natural killer phenotype. The results of this study suggest that the increase in natural killer cytotoxicity after opioid peptides injected once or for 14 days may result from an increased number of natural killer cells in the spleen.
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PMID:Effect of enkephalins and endorphins on cytotoxic activity of natural killer cells and macrophages/monocytes in mice. 919 78

To examine a functional relationship among pregnancy and central neurotensin and thermoregulatory and neuroimmune systems during heat stress, we monitored colonic temperature in six virgin female rats and six pregnant rats (9 to 11 days gestation) exposed to a microwave source. We also assayed splenic natural killer cell activity (NKCA), blood corticosterone (CS), and ACTH as indicators of the hypothalamic-pituitary-adrenal axis, beta-endorphin (beta-EP), and neurotensin (NT) in discrete brain regions. Additionally, we clarified the effects of intracerebroventricular (icv) administration of NT antiserum on these same responses in pregnant rats exposed to heat stress. Repeated-measures analysis of variance showed significant main effects of heat and pregnancy and a significant interactive effect on colonic temperature. Significant elevation in blood CS, ACTH, beta-EP, and NT in the hypothalamus and significant reductions in splenic NKCA and NT in the nucleus accumbens were produced by heat. In the experiment examining the effect of icv administration of NT antiserum, significant main effects of heat and administration and a significant interactive effect on colonic temperature were observed. Icv administration of NT antiserum increased splenic NKCA and decreased blood beta-EP. These results show that pregnancy enhances thermal homeostasis, suggesting central thermoregulatory mechanisms through NT in nucleus accumbens and hypothalamus in which placental or pituitary beta-EP may be involved. NT and beta-EP seem to play central roles simultaneously in heat-induced immunosuppression during pregnancy. Clarification for the effects of NT antiserum on beta-EP in virgin rats or manipulation of agents related to opioid system should be the focus of future work.
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PMID:Involvement of central neurotensin in thermoregulatory and neuroimmune function in pregnant rats exposed to heat. 929 63

To clarify the involvement of the opioid system in enhanced immunosuppression induced by heat stress during pregnancy, we examined the effects of heat exposure and intraperitoneal administration of opioid receptor antagonist naloxone on beta-endorphin (beta-EP) in blood, pituitary lobes, and placenta as well as splenic natural killer cell activity (NKCA) and placental steroids in pregnant rats at 15-16 days gestation. Two-way analysis of variance revealed significant increases in blood beta-EP induced by heat and naloxone and a significant interaction between heat and naloxone on blood beta-EP and progesterone (P). Whereas heat reduced NKCA, intraperitoneal administration of naloxone reversed it. Significant increases in blood and placental beta-EP induced by both heat and naloxone administration and a significant interaction on blood and placental beta-EP was observed. These results suggest that immunosuppression produced by heat stress during pregnancy is mediated by the opioid system. A positive correlation between beta-EP in blood and placenta during heat and naloxone administration suggests that increased placental beta-EP during heat results in hypersecretion of beta-EP into blood. P increased by heat during pregnancy may be involved in the immunosuppression.
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PMID:Opioid peptides mediate heat stress-induced immunosuppression during pregnancy. 953 Feb 32

To examine responses of natural killer cell activity (NKCA) to interleukin-1 beta (IL-1 beta) during pregnancy, we determined splenic NKCA as well as blood and brain indicators in virgin and pregnant rats (14 or 21 days gestation) with intracerebroventricular (i.c.v.) administration of IL-1 beta. NKCA was reduced and blood beta-endorphin (beta EP) was increased with the progress of pregnancy. I.c.v. administration of IL-1 beta reduced NKCA and corticotropin-releasing hormone (CRH) in the median eminence (ME), and increased beta EP in virgin rats, but did not change any parameters in pregnant rats with 21 days gestation. These data suggest that the immunosuppressive effect of central administration of IL-1 beta is blocked by pregnancy. CRH in the ME and opioid system seem to be involved in the inhibitory effect of pregnancy on IL-1 beta-induced immunosuppression.
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PMID:Central administration of interleukin-1 beta reduces natural killer cell activity in non-pregnant rats, but not in pregnant rats. 980 35


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