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)

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 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 purpose of this article is to provide information about the exercise-induced alterations of cellular immune parameters depending on the intensity related to the individual anaerobic threshold (IAT) and duration of exercise. Immunological parameters were differential blood counts (CD14, CD45), monocyte subpopulations (CD14, CD16), lymphocyte subpopulations (CD3, CD4, CD8, CD45RO, CD19, CD16, CD56, HLA-DR) and natural killer cells (CD3, CD16, CD56), oxidative burst activity of neutrophils, and phagocytosis of neutrophils (flow cytometry). The main results were: (a) "Moderate" exercise (duration < 2h at about 85% of the IAT corresponding to a lactate steady state at about 2 mmol.l-1, < 30 min at the IAT corresponding to a lactate steady state of 4 mmol.l-1) elicits lower changes in cell concentrations and hormonal responses than strenuous exercise [exhaustive exercise at 100% IAT or above; (exhaustive) long-term (> 2-3h) endurance exercise]. Similar investigations about cell functions to decide about the positive or negative nature of these observations will have to follow in the future. (b) The neutrocytosis following exercise is more dependent on the duration than on the intensity of exercise. Especially exercise sessions that lead to a strong incline of the adrenocorticotropic hormone, beta-endorphin and cortisol are associated with this neutrocytosis. (c) Neutrophils' function during the exercise-induced neutrocytosis indicated by phagocytosis and oxidative burst activity is unchanged or reduced following strenuous endurance exercise, whereas bacterial URTI leads to similar neutrophil counts but significantly increased cell activities indicating the diverse meaning of the leukocytosis in infections (primed cells, enhanced cell activity, stimulated defense mechanism) and following exercise (impaired cell function, suppressed defense mechanism). (d) Regular monocytes (early differentiation stage) are strongly recruited into the circulation during long-term aerobic exercise, whereas mature monocyte cell counts (premacrophages) increase most with highly intensive (an)aerobic exercise above the IAT. Infections induced a maturation from regular to mature monocytes as a response to the infectious antigenic stimulus, whereas exercise does not, indicating the diversity between change of cell counts and function. (e) Long-term endurance diverse meaning leads to increases of activated CD45RO+ T cells (memory cell phenotype) but compared to the incline of cell concentrations and activation levels (% HLA-DR+ T cells) during infections like infectious mononucleosis this effect is small indicating only minor effects on T cell function by exercise. The effect of single bouts of exercise on immune cell counts is large but the effects on the cell function is - i.e. compared to bacterial URTI - relatively small.
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PMID:The acute immune response to exercise: what does it mean? 912 61

This study was designed to test whether a single 50-mg dose of the opioid antagonist naltrexone hydrochloride, ingested 60 min before 2 h of moderate-intensity exercise (i.e., 65% peak O2 consumption), influenced the exercise-induced augmentation of peripheral blood natural killer cell cytolytic activity (NKCA). Ten healthy male subjects were tested on four occasions separated by intervals of at least 14 days. A rested-state control trial was followed by three double-blind exercise trials [placebo (P), naltrexone (N), and indomethacin] arranged according to a random block design. The indomethacin exercise trial is discussed elsewhere (S. G. Rhind, G. A. Gannon, P. N. Shek, and R. J. Shepherd. Med. Sci. Sports Exerc. 30: S20, 1998). For both the P and N trials, plasma levels of beta-endorphin were increased (P < 0.05) at 90 and 120 min of exercise but returned to resting (preexercise) levels 2 h postexercise. CD3(-)CD16(+)CD56(+) NK cell counts and NKCA were significantly (P < 0.05) elevated at each 30-min interval of exercise compared with correspondingly timed resting control values. However, there were no differences in NK cell counts or NKCA between P and N trials at any time point during the two trials. Changes in NKCA reflected mainly changes in NK cell count (r = 0.72; P < 0.001). The results do not support the hypothesis that the enhancement of NKCA during prolonged submaximal aerobic exercise is mediated by beta-endorphin.
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PMID:beta-Endorphin and natural killer cell cytolytic activity during prolonged exercise. is there a connection? 984 61

The opioid peptides are widely distributed throughout the body, and they are generated during stress and inflammatory reaction. Opioids are involved in the communication between the immune and neuroendocrine systems. In the present study we have investigated the ability of both met-enkephalin and beta-endorphin to stimulate and prime the human neutrophils for enhanced chemiluminescence (CL) and chemotaxis induced with fMLP, OZ or PMA. We have also tested the effect of beta-endorphin and met-enkephalin on CD11a, CD11b, CD18 and CD16 molecule expression on PMN in vitro. PMN from ten healthy donors were incubated in vitro with different concentrations of beta-endorphin or met-enkephalin, and the CL response was evaluated with luminometer. To assess the effect of opioid peptides on CD11a, CD11b, CD18 and CD16 molecule expression the whole blood samples were incubated with different concentrations of the opioids, then the white cells were labelled with respective PE-conjugated MoAb and evaluated by flow cytometry. We have shown that: (1) met-enkephalin and beta-endorphin at physiological concentrations relevant to that of in vivo (10(-8) and 10(-6) M) enhanced fMLP, PMA or OZ stimulated chemiluminescence and induced chemotactic response, (2) High concentrations of beta-endorphin (10(-3) M) or met-enkephalin (10(-5) M) decreased the CL response of PMN in vitro, (3) The opioid peptides at lower concentrations resulted in CD11b and CD18 molecule up-regulation on neutrophils. We may conclude that opioid peptides in physiological concentration are involved in neutrophil priming whereas in higher concentration exert immunosuppressive potency. Opioid peptides like inflammatory cytokines may prime the neutrophils inflammatory response.
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PMID:Priming effect of met-enkephalin and beta-endorphin on chemiluminescence, chemotaxis and CD11b molecule expression on human neutrophils in vitro. 1023 86

Beta-Endorphin has been reported to enhance natural killer (NK) activity in vitro. However, few studies have examined the precise regulation of the cytolytic stage of NK cells. We therefore investigated the regulation by beta-endorphin of cytotoxicity-associated molecules such as granzyme B, perforin, and Fas ligand (FasL) in human CD16(+) NK cells. On semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) assay, the granzyme B mRNA level apparently increased in CD16(+) NK cells from high responding subjects having ratios >1.5 for the LU(30) ratio. An increase in intracellular granzyme B molecules was also detected in CD16(+) NK cells by flow cytometry. On the other hand, perforin and FasL appeared not to be involved in regulation by beta-endorphin. These findings suggest that up-regulation of granzyme B expression may be involved in the enhancement of NK activity by beta-endorphin.
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PMID:Involvement of granzyme B expression in the enhancement of natural killer activity by beta-endorphin. 1072 15

It is well-established that bicycle exercise alters the endocrine and immune responses in men, but little information is available for women, especially middle-aged, post-menopausal women. The purpose of our study was to document the endocrine and immune reactivity to exhausting bicycle exercise in post-menopausal women, and to explore whether complaints of fatigue or low vigour are related to these exercise-induced responses. Thirteen healthy post-menopausal women participated in this study. We used a graded exercise protocol to study the kinetics of activation of the endocrine and immune system. We chose to examine hormones related to the hypothalamus-pituitary-adrenal (HPA) system such as adrenocorticotropin hormone (ACTH) and cortisol and hormones related to the pituitary such as prolactin (PRL) and growth hormone (GH). With regard to the immune system, we examined the natural killer (NK) cell activity and pokeweed (PWM)-induced lymphocyte proliferation in addition to changes in peripheral blood cell counts. Our results demonstrate that acute physical stress results in a strong release of ACTH, cortisol, GH and PRL. The bicycle test significantly increased the number of CD3+, CD4+, CD16/56+ (NK cells) and CD8+ cells in our group of post-menopausal women. Interestingly, NK activity did not increase significantly despite an increase in NK cell numbers. PWM-induced lymphocyte proliferation did not change either. In addition, our data support the hypothesis that low vigour in post-menopausal women interferes with the endocrine and immune responses to exhausting exercise. In women with complaints of low vigour we found lower cortisol responses and higher increments in the proliferative capacity of lymphocytes as compared to those with high vigour scores. NK activity was unrelated to exhaustive mood states. These data indicate that endocrine as well as immune system activity changes in response to exhausting exercise in middle-aged, post-menopausal women. In addition, exhaustive mood states may contribute to cortisol responses and function of peripheral immune cells in post-menopausal women following exhausting exercise.
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PMID:An exploratory study into the effect of exhausting bicycle exercise on endocrine and immune responses in post-menopausal women: relationships between vigour and plasma cortisol concentrations and lymphocyte proliferation following exercise. 1153 Oct 39

In order to characterize a wide spectrum of leukocyte functions with clinically applicable procedures, 0.06 ml each of heparinized whole blood was stimulated in triplicate for 4h with phytohemagglutinin (T cell stimulator), heat aggregated IgG (IgG Fc receptor stimulator), lipopolysaccharide (toll-like receptor (TLR)-4 stimulator), zymosan (TLR-2 stimulator), monoclonal antibody against T-cell receptor alpha/beta chain, recombinant interleukin-2, and solvent controls, then 32 different leukocyte function-associated mRNAs were quantified by the method reported previously (Mitsuhashi et al. Clin. Chem. 2006). Two control genes (beta-actin, beta-2-microglobulin) were not affected by these stimulations, whereas the induction of CCL chemokines-2, 4, 8, 20, CXCL chemokines-3, 10, interleukin (IL)-8 (markers of leukocyte accumulation/recruit), granzyme B, perforin 1, tumor necrosis factor superfamily-1, 2, 5, 14, 15, CD16 (markers of cell killing), IL10, transforming growth factor beta 1 (humoral factors of immune suppression), forkhead box P3, CD25, arginase (cellular markers of immune suppression), IL2, IL4, interferon-gamma, IL17 (markers of various subsets of T helper cells), granulocyte-macrophage colony-stimulating factor (marker of antigen presenting cells), immunoglobulin heavy locus (marker of B-cells), vascular endothelial growth factor (marker of angiogenesis), pro-opiomelanocortin (marker of local pain), and CD11a mRNA (marker of leukocyte adherence to endothelium) were identified by these stimulations. The blood volume in this assay was 1.44 ml, and 4 h' incubation in whole blood was physiological. Using triplicate aliquots of whole blood for both stimulant and solvent control, statistical conclusion was drawn for each stimulant for each mRNA. The method introduced in this study will be a new paradigm for clinical cellular immunology.
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PMID:Ex vivo simulation of leukocyte function: stimulation of specific subset of leukocytes in whole blood followed by the measurement of function-associated mRNAs. 2095 4