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 opioid peptides methionine enkephalin (M-ENK) and beta-endorphin (beta-END) (1 x 10(-5)-1 x 10(-11) mg/ml) were investigated for their effect on the PHA (1:500, 1:750 or 1:1000) induced proliferative response of old and young Wistar rat splenic lymphocytes in vitro. The different effects in young and old rats on proliferative response to PHA were determined. The results showed that MENK and beta-END significantly enhanced the proliferative response to PHA in young rats, while enhancement by M-ENK and beta-endorphin (PHA 1:750, 1:1000) was not observed in old rats. The PHA-induced proliferative response was 30%-40% lower in old rats than in young rats. Our results suggest an altered response to neuro-immunomodulation with age. The in vitro effect of ENKs on phagocytosis was also studied. The results indicated that LENK (10(-4)-10(-6) mg/ml) and MENK (10(-2)-10(-4) mg/ml) could stimulate the phagocytosis of peritoneal macrophages from Balb/c mice.
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PMID:[Ageing suppresses the enhancement of T cell mitogenesis by opioid peptides and enkephalins increase phagocytosis of murines macrophage]. 139 43

We measured the concentrations of beta-endorphin in resting peripheral blood mononuclear cells obtained from normal subjects of different ages and from age-matched patients with Down's syndrome or Alzheimer's disease. We also measured beta-endorphin concentrations in peripheral blood mononuclear cells obtained from subjects of different ages after treatment with PHA or serotoninergic drugs. The results show that in normal subjects the concentrations of the peptide increase after 30 years of age and remain constant up to 99 years. After stimulation with PHA, the release of beta-endorphin in cells from subjects older than 30 years increases, leading to a decrease in contents, whereas it is unchanged in younger subjects. In patients with Down's syndrome or Alzheimer's disease, beta-endorphin concentrations in peripheral blood mononuclear cells behave similarly to those in age-matched normal subjects. Treatment in vivo with the serotoninergic agonist chlorimipramine induces an increase in beta-endorphin concentrations in peripheral blood mononuclear cells that is significantly greater in subjects over 30 years old than in younger subjects.
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PMID:Beta-endorphin concentrations in resting peripheral mononuclear cells and after treatment with PHA or serotoninergic drugs in human aging, Alzheimer's disease, and Down's syndrome. 148 61

Human peripheral blood mononuclear cells are analyzed for preproenkephalin gene expression and peptide processing. Met-enkephalin immunoreactivity as detected with a specific antiserum is found in the cytoplasm of monocytes but not in T lymphocytes. Secretion of met-enkephalin was analyzed with an RIA that is specific for the met-enkephalin pentapeptide. Unfractionated PBMC spontaneously released 40 pg/ml met-enkephalin and this increased two- to fourfold after stimulation with PHA. Lower levels (less than 100 pg/ml) of met-enkephalin were detected in supernatants from purified T cells that were activated with PHA and IL-2. In contrast, stimulation of purified monocytes with LPS or PMA resulted in the release of up to 600 pg/ml of the processed peptide. To examine whether T cells can produce met-enkephalin precursor peptides, T cell conditioned media were treated with trypsin and carboxypeptidase-B, which is known to release met-enkephalin from the propeptide. This increased levels of met-enkephalin to 400 pg/ml, indicating that lymphocytes secrete the propeptide but do not process it to met-enkephalin. The 1.4-kb preproenkephalin mRNA is detected in activated blood mononuclear cells and in purified monocytes and T cells. To determine whether monocytes or lymphocytes express met-enkephalin in vivo, lymphoid tissues were analyzed by immunohistochemistry. In human spleen tissue, positive cells were found in the red pulp but not in the follicles, which is also consistent with met-enkephalin expression in monocytes. In summary, these results show that human peripheral blood mononuclear cells express preproenkephalin mRNA and that monocytes, but not T cells, process the propeptide to metenkephalin.
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PMID:Differential processing of proenkephalin-A by human peripheral blood monocytes and T lymphocytes. 188 71

Two trials were conducted to assess the effects of adrenocorticotropin (ACTH) and dietary ascorbic acid (AA) on cutaneous basophil hypersensitivity (CBH) to phytohemagglutinin (PHA-P) in chickens. Broiler chicks received AA at levels of 0, 150, or 300 mg/kg of feed (ppm) continuous from hatching. At 6 to 7 wk of age, birds from each AA group received either 2 IU ACTH/100 g of body weight, 4% gelatin, or no ACTH or gelatin injections. Injections were given 12 h prior to, at the time of, and at 12 and 24 h after an intradermal wattle injection with PHA-P. Responses to PHA-P were determined as wattle indices. Injections of ACTH reduced body weight gain in both trials and decreased relative bursa weight in Trial 1. Injections of ACTH and dietary AA increased plasma cholesterol in both trials. Peak CBH wattle response occurred at 24 h post PHA-P injection. Injections of ACTH decreased mean wattle index at 18 and 36 h post PHA-P injection in Trial 1 and 18 and 24 h post PHA-P injection in Trial 2. The addition of AA ameliorated the ACTH-mediated suppression of CBH in a dose-related manner.
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PMID:Effect of adrenocorticotropin and dietary ascorbic acid on cutaneous basophil hypersensitivity to phytohemagglutinin in chickens. 283 37

Immunosuppression is frequently observed after traumatic injury, and is associated with the subsequent development of sepsis. Although a number of factors such as age, nutritional status, and the degree of injury have been related to the severity of the immunosuppression that occurs, the physiologic alterations leading to immunosuppression are not well defined. We hypothesized that changes in the endogenous opiate peptides, such as beta-endorphin, might contribute to changes in the immune system following injury. Levels of circulating beta-endorphin, responsiveness to the mitogen PHA, and the frequency of circulating T11, T4, and T8 cells were measured in trauma patients hospitalized in a surgical intensive care unit. beta-endorphin levels were elevated during the first 4 days after trauma (134.1 +/- 22.5 vs. 49.3 +/- 4.3 pg/ml, mean +/- S.E., patient vs. control; p less than 0.001). During the same time period patient PHA response (10,852 +/- 3,775 vs. 28,147 +/- 12,078; p less than 0.05), and the per cent of T4 positive (31.2 +/- 2.6 vs. 47.0 +/- 1.4; p less than 0.001) cells were lower than controls. These parameters were not significantly different from control values when measured at later times. Thus we conclude there is a temporal association of depressed immune parameters and elevated beta-endorphin levels after traumatic injury.
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PMID:Elevation of circulating beta-endorphin levels with concomitant depression of immune parameters after traumatic injury. 293 93

Beta-endorphin (10(-11)-10(-9) M) has been shown to induce naloxone-independent depression of the proliferative activity of human peripheral lymphocytes (HL), stimulated by pokeweed mitogen without affecting PHA-stimulated HL proliferation. Beta-endorphin (10(-10)-10(-7) M) also caused changes in HL cAMP level, that were blocked by naloxone. Marked individual sensitivity to beta-endorphin effects has been noted. It has been also shown that a bone marrow preparation, stimulating antibody production (myelopeptides), causes naloxone-independent depression in the proliferative activity of HL, stimulated by PHA and pokeweed mitogen, as well as naloxone-blocked decrease in cAMP HL level. It has been concluded that beta-endorphin interacts with several types of opiate lymphocyte receptors and that opioids, contained in myelopeptides, are involved in the realization of myelopeptide effect on lymphocytes.
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PMID:[Effect of beta-endorphin and myelopeptides on the cAMP level and proliferation of lymphocytes in vitro]. 302 14

beta-Endorphin is an opioid peptide synthesized in the pituitary, hypothalamus, and immunocytes, known to affect immune responses both when added in vitro and when its synthesis is increased in vivo (e.g., during stress). We show here that, similar to its concentrations in peripheral blood mononuclear cells, the release of the opioid peptide from these cells after stimulation with polyclonal mitogens such as PHA or Con-A is also age dependent. Moreover, the effect of both mitogens on Ca2+ homeostasis changes with age. Finally, the ionophore ionomycin and the Ca2+ ATPase blocker thapsigargin induce the same age related effect on beta-endorphin release. For these reasons, we suggest that calcium homeostasis might be important for the differences observed in the release of the opioid from cells obtained from younger (< or = 30 years) or older (> or = 45 years) volunteers.
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PMID:Age-related changes in mitogen-induced beta-endorphin release from human peripheral blood mononuclear cells. 747 5

The effects of opioid peptides on immune responses were investigated. It was found that beta-endorphin (beta-END) can depress proliferative responses to PHA in rat splenocytes but enhance those in mice, and it could also inhibit the plaque-forming cell (PFC) response to sheep red blood cells when mouse splenocytes immunized in vivo were cultured in vitro with the peptide. The peptide antagonist naloxone was able to reverse beta-END suppression of the PFC response. The data indicate that beta-END suppresses antibody production or secretion via a specific opioid-receptor-mediated mechanism.
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PMID:Effects of beta-endorphin on phytohemagglutinin-induced lymphocyte proliferation and mouse plaque-forming cell response via an opioid receptor mechanism. 771 65

We investigated beta-endorphin (BE) content in an HIV-infected cell line and in peripheral blood mononuclear cells (PBM) from HIV-positive subjects. HIV infection increased BE content in HuT78 cell line compared to uninfected cells. Accordingly, BE content was greater in HIV-positive subjects than in healthy controls, both in fresh PBM and in mitogen-stimulated or unstimulated cultured cells. Further, in PHA-stimulated cultures, BE increase was correlated with disease progression. Opioids are known to decrease immune responsiveness in vivo, and it may be that the increased BE concentrations contribute to HIV-associated immune deficiency. In HIV-positive subjects, but not in healthy controls, intracellular BE concentration was positively correlated with PHA-induced PBM proliferation. The latter data suggest an alternative explanation: that the increased BE content represents a paradoxical response of the host in an attempt to balance virus-induced immunodepression. Thus, BE may be important in fine-tuning of the immune response with its up- and downregulation dependent upon differences in immune status.
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PMID:Beta-endorphin content in HIV-infected HuT78 cell line and in peripheral lymphocytes from HIV-positive subjects. 798 93

A peptide inhibiting either corpuscolate or purified PKC has been identified from microsomes of PHA-activated human PBMC but it is not detectable in microsomes of resting PBMC. The peptide was obtained from a microsomal preparation in an oligomeric form that could be transformed into a monomeric form by beta-MSH. The active peptide (IN) was retained on a PC-11 chromatographic column and could be eluted with NaCl. IN is ineffective on PKC-dependent protamine phosphorylation of protamine and on Ca2+ and phospholipid-independent activity generated by mild hydrolysis with trypsin of PKC. Ca2+ binding is permissive for IN activity. IN inhibits particulate PKC in PHA-activated PBMC, but is ineffective after TPA activation. All these data indicate that IN acts at the regulatory domain of PKC.
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PMID:Identification of a novel protein kinase C inhibitor in microsomes from phytohaemagglutinin activated human peripheral blood mononuclear cells. 836 75


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