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)

The release of neuropeptides, such as substance P (SP) and somatostatin (SOM), from primary sensory nerve fibers has been implicated in the modulation of local immune responses in surface tissues, such as the skin, the pulmonary airways, and the gastrointestinal mucosa. We have investigated the influence of six neuropeptides substance P (SP), somatostatin (SOM), substance K (SK), vasoactive intestinal peptide (VIP), bombesin (BOM), and adrenocorticotropic hormone (ACTH) on the proliferation of resting and partially stimulated human peripheral blood mononuclear leukocytes (PBMLs) and T lymphocytes. Neuropeptides in concentrations from 10(-7) to 10(-12) M were added to either resting or partially stimulated cells [interleukin-2 (IL-2), concanavalin A (Con A), and phytohemagglutinin (PHA)]. Cellular proliferation was assessed by incorporation of 3H-thymidine after 72 h. With the exception of SP, no significant effect of any of these neuropeptides on 3H-thymidine incorporation was found. In resting cells, 10(-9) MSP elicits an 80...maximal increase of 3H-thymidine incorporation, whereas no statistically significant effect on partially stimulated leukocytes was found. These results contradict a previous report on a significant mitogenic effect of SP on partially stimulated T cells. Considering the very minimal effect of SP on resting cells and, particularly, the absence of an effect on partially stimulated cells, we would question a significant modulatory role for SP and the five other neuropeptides in the proliferation of immunocompetent cells in skin.
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PMID:Effect of neuropeptides present in skin on the proliferation of human peripheral blood mononuclear cells and T cells. 246 35

Pituitary cells were shown to release corticotropin (ACTH) in response to interleukin-2 (IL-2) and to express a protein that is related to the alpha-chain of the IL-2 receptor (IL-2R). The alpha-chain-like molecule was bound by a rat monoclonal antibody to the murine IL-2 receptor as well as to IL-2. Sodium dodecylsulfate-polyacrylamide gel electrophoretic analysis of the affinity-purified material from pituitary cells demonstrated a protein which was similar to that which was isolated from activated splenocytes. Thus, IL-2 and its receptor may be one of several hormone-receptor pairs utilized by both the immune and neuroendocrine systems for intersystem communication.
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PMID:Interleukin-2 induction of ACTH secretion: presence of an interleukin-2 receptor alpha-chain-like molecule on pituitary cells. 253 95

To assess cellular immune status and the hypothalamic-pituitary (HP) axis in patients with major depression, we examined peripheral blood mononuclear cells (PBMC) and measured the plasma levels of cortisol, adrenocorticotropin hormone (ACTH), growth hormone (GH), and prolactin (PRL). Twenty patients with major depression were compared with 20 control subjects matched for age, sex, and race. The dose-response curves for concanavalin-A (Con-A) and phytohemagglutinin (PHA) stimulation were not significantly different between the two groups. The patients had decreased Con-A-stimulated T-lymphocyte proliferation when compared to the control subjects, but only at the lowest suboptimal concentration of Con-A. None of the four concentrations of PHA-stimulated proliferation were different between the two groups, neither was PHA-induced interleukin-2 production. Within the patient group only, plasma prolactin (PRL) correlated significantly with stimulated lymphocyte proliferation using two optimal concentrations of PHA and one optimal concentration of Con-A, when the proliferation was expressed using the stimulation index.
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PMID:Mitogen-stimulated lymphocyte proliferation and pituitary hormones in major depression. 254 31

Observations of neuropsychiatric changes in patients receiving interleukin-2 (IL-2) led us to examine the effects of IL-2 administration on the stress-related hormones, beta-endorphin, ACTH, cortisol, and CRH. We evaluated 30 cancer patients who received immunotherapy with IL-2 or IL-2 plus lymphokine-activated killer (LAK) cells. Blood samples were taken immediately before and 4 and 8 h after infusion of IL-2 or IL-2 plus LAK cells. IL-2 stimulated increased hormone levels 4 h after infusion compared with those before therapy and with basal levels in normal volunteers at the following magnitudes: beta-endorphin, 10-fold; ACTH, 20-fold; and cortisol, 2-fold. The effect of IL-2 was not altered in patients also receiving LAK cells. An effect of treatment course was noted, with higher stimulated values seen 4 h after IL-2 in the second treatment course compared with those after the first course [change (delta) in beta-endorphin, 101 vs. 11 fmol/mL; delta ACTH, 138 vs. 8 pmol/L; delta cortisol, 414 vs. 218 nmol/L]. We conclude that IL-2 treatment induces the release of neuroendocrine hormones and that a significant increase in hormonal stimulation occurs upon reexposure to IL-2.
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PMID:The neuroendocrine effects of interleukin-2 treatment. 254 65

We compared adrenocorticotropin-releasing activities of several interleukins in a homologous or heterologous in vivo system. Intravenous injection of rat interleukin-1 alpha significantly increased plasma adrenocorticotropin in conscious, freely-moving rats 30 min after the injection, and the effect was 10 times greater than that of human interleukin-1 alpha. Rat interleukin-2 affected plasma adrenocorticotropin in a much slower manner and increased its levels significantly 120 min after the injection. Human interleukin-2 had no effect on plasma adrenocorticotropin. Thus, species difference in the experimental system should be considered to assess the physiological significance of cytokines in the neuroendocrine system.
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PMID:Adrenocorticotropic hormone-releasing activities of interleukins in a homologous in vivo system. 255 22

The effect of the opiate peptide, beta-endorphin (beta-END), on the autologous and allogeneic mixed lymphocyte reaction was examined. Physiologic concentrations of beta-END augmented proliferation of the autologous mixed lymphocyte reaction (AMLR) but the allogeneic MLR was not altered. Alpha-endorphin (alpha-END) was ineffective. Pre-incubation of the stimulator subset (i.e., B cells and macrophages) with 10(-8) M beta-END followed by addition to AMLR culture without additional opiate peptide did not produce augmentation. The beta-END-induced augmentation of the AMLR was partially inhibited by the opiate antagonist naloxone. beta-END augmentation was not due to increased secretion of interleukin-2. When prostaglandin E2 (PGE2) was added to AMLR cultures wherein the stimulator cell fraction was vigorously depleted of adherent cells, suppression was observed which could be reversed by the addition of beta-END (10(-8) M). The potential mechanisms producing the increased proliferative response during the AMLR are discussed.
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PMID:Modulation of the autologous mixed lymphocyte reaction by beta-endorphin. 282 56

Beta-endorphin has been reported to enhance T lymphocyte proliferation and cytolytic activity. In this report, it is demonstrated that beta-endorphin enhances the production of the T cell lymphokine, interleukin-2, from mitogen-stimulated, unfractionated murine splenocytes, as well from a cloned T cell line. The enhancement is naloxone irreversible and dependent on the integrity of the C-terminal amino acids, though the N-terminal amino acids appear to contribute to the potency of the enhancement. The data suggest that beta-endorphin interacts with a nonopioid receptor that has specificity characteristics similar to a nonopioid beta-endorphin receptor described in the central nervous system.
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PMID:Beta-endorphin enhances interleukin-2 (IL-2) production in murine lymphocytes. 283 33

We examined the effect of rotation-induced stress on (1) growth of lymphosarcoma tumors; (2) interleukin-2 (IL-2) production; (3) T cell subset distribution; and (4) cytotoxic T cell (CTL) function. In addition, we examined the levels of corticosterone and beta-endorphin as possible mediators of stress-induced immune alterations. Rotation stress induced progressive lymphosarcoma growth, while unstressed mice showed tumor regression after 2 weeks of growth. IL-2 production and CTL activity in stressed animals were significantly lower than controls during the first 2 weeks after initiation of stress. Spleen lymphocytes from stressed and control mice bearing the L3T4 antigen (helper/inducer T cell marker) remained unchanged, while in peripheral blood such cells decreased in stressed but not control animals. This latter pattern was also observed in Lyt 2 positive (suppressor/cytotoxic) cells of both spleen and peripheral blood. Corticosterone levels were elevated for an extended period following initiation of stress, while beta-endorphin levels remained similar to those of the controls. Although these data do not directly establish a causal link between immunoinhibition and tumor growth, they clearly demonstrate that stress inhibits a number of cell-mediated immune functions that may be relevant in this regard.
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PMID:Stress-induced decline in immune responsiveness in C3H/HeJ mice: relation to endocrine alterations and tumor growth. 326 57

We are interested in the characterization of the effects of alcohol on human T-cell activation, maturation, and migration, because this cell population is crucial in the initiation, regulation, and propagation of cellular immunity. We and others have described the effects of both acute and chronic exposure of human immune cells to ethanol (EtOH) in vitro. Herein, we briefly, review these reports and expand this body of literature with the inclusion of new data recently obtained in our laboratory. We confirm the blunting effects of EtOH on the production of interleukin-2 and mitogen proliferative response following T-cell mitogen stimulation, and on the expression of membrane markers of activation. We show that EtOH significantly alters the expression of the CD4 cell-associated marker of activation, CD26. We report the effect of EtOH on the expression of the homing receptor CD62L by CD4+ cells, and on their ability to adhere by a CD18-mediated process to a defined cellular substratum. Furthermore, we demonstrate the effects of EtOH and EtOH and beta-endorphin pretreatment on the activation of CD4+ lymphocytes endowed with the homing receptor CD62L.
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PMID:Alcohol modulation of human normal T-cell activation, maturation, and migration. 757 70

Previous studies of psychopathological populations and populations challenged by significant life events have shown that high levels of anxiety and depression are associated with impaired cellular immunity. However, less is known about the sources and psychoimmunological relevance of subclinical variations in distress in healthy populations faced with typical levels of life stress. In the present study, we examined the relations of state distress to T-cell function and in vivo cytokine levels in 40 male college freshmen on two occasions. In addition, we assessed the possible contribution of dispositional determinants of distress to immune-related differences in mood. Relative to characteristically less anxious subjects, subjects who were characteristically more anxious (but subclinically anxious) had more anxious mood and had significantly lower lymphocyte proliferative responses to the mitogen concanavalin A (Con A) as well as lower levels of circulating interleukin-1 beta. In addition, subjects with more negative attributional styles for bad events exhibited reduced Con A-stimulated T-cell responses and lower levels of circulating interleukin-2. Finally, subjects who were more depressed (but subclinically depressed) also had reduced blastogenic responses. Individual differences in cortisol and beta-endorphin were not shown to mediate these relationships. The present study provides evidence that dispositionally related variations in distress in psychiatrically healthy, relatively unstressed college males have immunological correlates that suggest altered T-cell and macrophage activity.
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PMID:Reduced cytokine levels and T-cell function in healthy males: relation to individual differences in subclinical anxiety. 769 16


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