Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixteen subjects (male, age: 26.3 +/- 3.5 years, weight: 75.1 +/- 6.5 kg, maximal oxygen uptake: 53.6 +/- 6.7 ml.min-1.kg-1) performed endurance exercises at 100% (exhaustive), and 85% (limited) of the individual anaerobic threshold [IAT; workload (100% IAT): 3.00 +/- 0.50 W.kg-1, duration of both exercises: 87 +/- 21 min]. Before (b), immediately (0 p), 60 min (60 p), 120 min (120 p) and 24 hours (24 hp) after exercise, leucocyte subpopulations (flow cytometry) as well as epinephrine, norepinephrine, cortisol, beta-endorphin and ACTH were determined. At 0 p, 60 p and 120 p, granulocytes were significantly higher at 100% IAT than at 85% IAT, lymphocytes and monocytes did not differ. At 60 p and 120 p, granulocytes had highest, lymphocytes lowest values. CD8(+)- and CD16(+)-lymphocytes showed greater changes than CD3(+)-, CD4(+)-, CD19(+)-lymphocytes and were significantly higher at 100% IAT than at 85% IAT (0 p). Epinephrine and norepinephrine were significantly higher at 100% IAT than at 85% IAT. Cortisol, ACTH and beta-endorphin increased at 100% IAT, but not at 85% IAT (0 p). Significant correlations were calculated for cortisol (0 p) versus granulocytes (60 p, 120 p) at 100% IAT. Epinephrine did not correlate to increases of lymphocytes or lymphocyte subpopulations. In conclusion, increases of granulocytes, CD16(+)- and CD8(+)-lymphocytes are dependent on the intensity of endurance exercises and precise definition of the individual workload is important. The increase of granulocytes after exercise is partly due to increased levels of cortisol. Increased cell numbers of lymphocytes, especially CD16(+)-cells, did not correlate to increased levels of catecholamines.
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PMID:Immunoregulatory hormones, circulating leucocyte and lymphocyte subpopulations before and after endurance exercise of different intensities. 132 59

The neuropeptide beta-endorphin can modulate the response of T and B cells to mitogenic or antigenic stimulation. In the present report we describe a novel mechanism by which beta-endorphin can interfere with T cell activation. It is shown here that beta-endorphin can modulate the phorbol ester-induced phosphorylation of the gamma chain of the CD3 complex. The effect of beta-endorphin is dose dependent and appears to be mediated via interaction of beta-endorphin with an opiate receptor on lymphocytes. Evidence is presented that the modulatory effect of beta-endorphin is specific for the phosphorylation of the CD3 gamma chain. beta-Endorphin does not affect the phosphorylation of total cell protein, nor does it have any effect on the phosphorylation of the CD4 determinant on T cells. The possible consequence of a change in CD3 gamma chain phosphorylation is discussed.
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PMID:The phosphorylation of the CD3 gamma chain of T lymphocytes is modulated by beta-endorphin. 214 Jul 92

The authors provide the results of an analysis of the interrelation between the immunologic and biochemical parameters in 6 groups of patients suffering from facial pains or headaches (a total of 153 patients). Significant correlations were revealed in the patients' groups with trigeminal neuralgia and periodic migrainous Horton's neuralgia. The main attention was concentrated on the following parameters: IgA in the serum, secretory IgA in the patients' saliva, % CD4 of lymphocytes and histamine concentration in the peripheral blood, concentration of beta-endorphin in the plasma, catecholamine content in the urine.
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PMID:[Immunologic and biochemical changes in patients with cranio-facial pain]. 216 79

The studies have clearly demonstrated that binding sites for opioid peptides, beta-endorphin, and methionine-enkephalin exist on T lymphocytes. beta-Endorphin appears to be immunodepressant, whereas methionine-enkephalin is immunostimulant. Both in vitro and in vivo studies have shown that methionine-enkephalin can influence some immune functions. Since in vitro modification of immune function requires very low concentrations, it is reasonable to believe that methionine-enkephalin plays a physiological role in the immune system. Although not well established, methionine-enkephalin appears to activate T lymphocytes via opioid receptors and triggers a series of intracellular signals leading to the activation of receptors for interleukin-2 (IL-2), OKT10, and active sheep T red blood cell receptors. Methionine-enkephalin enhances the activity of NK cells and induces the production of IL-2, which in turn may recruit and activate other T-cell subsets like CD3 and CD4. Methionine-enkephalin also enhances mitogen-induced proliferation of lymphocytes. Since preliminary studies with methionine-enkephalin in ARC patients have provided beneficial effects by the improvements in their symptoms, it will be worthwhile to extend these observations to a larger number of patients with ARC and AIDS. Finally, it appears that some endogenous opioid peptides and their analogs, in addition to methionine-enkephalin, may provide therapeutic benefits not only in ARC and AIDS but also in other immunodeficient states.
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PMID:Opioid peptides, receptors, and immune function. 217 24

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

Cocaine is reported to be immunotoxic. The biochemical mechanisms responsible for the immunopharmacological outcomes of cocaine in vivo and in vitro remain, however, to be fully elucidated. Our experimental data confirm that exposure of normal human T cells to micromolar concentrations of cocaine modulates T-cell responses to stimulation by a variety of stimuli, and indicate that cocaine impairs early activation events during CD4+ but not CD4- T-cell stimulation. Pre-incubation of enriched CD4+ T-cell subpopulations that express the homing receptor CD62L with nanomolar concentrations of the endogenous opioid peptide beta-endorphin leads to a more severe impairment of activation than that noted following pre-incubation with micromolar concentrations of cocaine alone. These findings begin to elucidate the molecular and cellular mechanisms of the immunopathology of cocaine. Our data support the proposition that cocaine abuse may place cocaine-abuser HIV-seropositive individuals at increased risk of opportunistic infections.
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PMID:Cocaine blunts human CD4+ cell activation. 785 54

The hypothesis that sleep deprivation depresses immune function was tested in 20 adults, selected on the basis of their normal blood chemistry, monitored in a laboratory for 7 d, and kept awake for 64 h. At 2200 h each day measurements were taken of total leukocytes (WBC), monocytes, granulocytes, lymphocytes, eosinophils, erythrocytes (RBC), B and T lymphocyte subsets, activated T cells, and natural killer (NK) subpopulations (CD56/CD8 dual-positive cells, CD16-positive cells, CD57-positive cells). Functional tests included NK cytotoxicity, lymphocyte stimulation with mitogens, and DNA analysis of cell cycle. Sleep loss was associated with leukocytosis and increased NK cell activity. At the maximum sleep deprivation, increases were observed in counts of WBC, granulocytes, monocytes, NK activity, and the proportion of lymphocytes in the S phase of the cell cycle. Changes in monocyte counts correlated with changes in other immune parameters. Counts of CD4, CD16, CD56, and CD57 lymphocytes declined after one night without sleep, whereas CD56 and CD57 counts increased after two nights. No changes were observed in other lymphocyte counts, in proliferative responses to mitogens, or in plasma levels of cortisol or adrenocorticotropin hormone. The physiologic leukocytosis and NK activity increases during deprivation were eliminated by recovery sleep in a manner parallel to neurobehavioral function, suggesting that the immune alterations may be associated with biological pressure for sleep.
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PMID:Leukocytosis and natural killer cell function parallel neurobehavioral fatigue induced by 64 hours of sleep deprivation. 791 Jan 71

The effects of glucocorticoid (GC) treatment on the mature immune and neuroendocrine system are known to be reversible. However, prenatal GC exposure may have irreversible consequences on the development of the newborn. In this study, possible long-lasting effects of short-term prenatal GC treatment were examined on the developing thymus, spleen and hypothalamo-pituitary adrenal axis (HPA axis). Female rats were given dexamethasone (DEX, 400 micrograms, i.p.) on day 17 and 19 of pregnancy and offspring was studied at several time intervals (1-20 days) after birth, for examination of thymus, spleen, hypothalamus and blood plasma. Examination of thymus and spleen revealed that prenatal exposure to DEX resulted in decreased T cell numbers in thymus and spleen on day 1 after birth. Thymus regeneration after DEX exposure both during pregnancy and in adult life was completed after 24 days. However, the kinetics of regeneration of the thymi after prenatal DEX exposure were different from that seen after DEX in adult life. Whereas DEX treatment during pregnancy resulted in an increased ratio of CD4+/CD8- thymocytes over CD4-/CD8+ thymocytes compared to control groups on day 7 and day 20 after birth (time X treatment interaction; P < 0.05), DEX treatment in adult life did not change this ratio. T cell numbers in the spleen were significantly decreased at all neonatal ages studied. Regarding the hypothalamus, prenatal exposure to DEX altered the pattern of neonatal changes in peptide expression in corticotropin-releasing hormone neurons, with a selective reduction in CRH storage in the median eminence (7 and 9 days after birth) and an increase in AVP storage (9 and 20 days after birth). The ratio of AVP over CRH was significantly increased at all developmental ages studied. No effects were seen on basal ACTH and corticosterone levels in plasma. In conclusion, the kinetics of thymus regeneration after DEX exposure during pregnancy were different from that seen after DEX exposure in adult life. Prenatal DEX exposure also seemed to delay the migration of T cells into the spleen. Furthermore, prenatal DEX treatment exerted major effects on hypothalamic CRH neurons that maintained for at least 20 days after birth, which points towards an enhanced stress responsiveness of the HPA axis in later life.
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PMID:Effects of short-term dexamethasone treatment during pregnancy on the development of the immune system and the hypothalamo-pituitary adrenal axis in the rat. 855 Aug 16

The emerging concept of opioid peptides as a new class of chemical messengers of the neuroimmune axis and the presence of a number of immunological abnormalities in infantile autism prompted us to correlate biological (hormonal and immunological) determinations and behavioural performances during treatment with the potent opiate antagonist, naltrexone (NAL). Twelve autistic patients ranging from 7 to 15 years, diagnosed according to DSM-III-R, entered a double-blind crossover study with NAL at the doses of 0.5, 1.0 and 1.5 mg/kg every 48 hours. The behavioural evaluation was conducted using the specific BSE and CARS rating scales NAL treatment produced a significant reduction of the autistic symptomatology in seven ("responders") out of 12 children. The behavioural improvement was accompanied by alterations in the distribution of the major lymphocyte subsets, with a significant increase of the T-helper-inducers (CD4+CD8-) and a significant reduction of the T-cytotoxic-suppressor (CD4-CD8+) resulting in a normalization of the CD4/CD8 ratio. Changes in natural killer cells and activity were inversely related to plasma beta-endorphin levels. It is suggested that the mechanisms underlying opioid-immune interactions are altered in this population of autistic children and that an immunological screening may have prognostic value for the pharmacological therapy with opiate antagonists.
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PMID:Opioid-immune interactions in autism: behavioural and immunological assessment during a double-blind treatment with naltrexone. 902 57

Hormones of the hypothalamic-pituitary-adrenal (HPA) axis are connected closely with immune measures. To investigate whether Cushing's syndrome (CS) is associated with immune dysregulation, we compared the percentage of specific lymphocyte subsets as well as natural cell activity (NKCA) in 48 patients with Cushing's syndrome and 48 age- and sex-matched normal controls. Lymphocyte subset analysis included the percentage of lymphocytes expressing CD3 (total T), CD4 (T helper/inducer), CD8 (T suppressor/cytotoxic) and CD56 (NK cell) antigens. Baseline plasma concentrations of cortisol, ACTH and beta-endorphin as well as 24 h urinary-free cortisol (UFC) levels also were determined. Results indicated a decrease in the percentage of CD4+ cells (p < 0.05), an increase in percentage of CD8+ cells (p < 0.05), a decrease in CD4/CD8 ratios (p < 0.01), and a reduction in NKCA (p < 0.05) in patients with CS compared to matched controls. We also found significant negative correlations between NKCA on the one hand and 24 h UFC (p < 0.05) and plasma beta-endorphin (p < 0.05) on the other. These results indicate there is immune dysregulation in CS patients which can be explained in part by an increase in HPA-axis hormones.
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PMID:Immune regulation in Cushing's syndrome: relationship to hypothalamic-pituitary-adrenal axis hormones. 904 43


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