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)

During development of adjuvant-induced arthritis (AA) in the rat, pituitary pro-opiomelanocortin (POMC) mRNA expression was increased. Pituitary POMC mRNA was much higher following adrenalectomy and AA. Spleen POMC mRNA also increased with a similar time kinetics, although the levels in the spleen were much lower than those in the pituitary. In control animals, spleen interleukin-1 beta (IL-1 beta mRNA) was undetectable, whereas AA led to the accumulation of IL-1 beta mRNA and the highest levels were seen in the adrenalectomised AA group. Thymic IL-1 beta expression was also increased in AA animals. These results suggest that AA leads to the activation of both the neuroendocrine and the immune systems and the interaction between these systems may play a role in this disease state.
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PMID:Response of pituitary and spleen pro-opiomelanocortin mRNA, and spleen and thymus interleukin-1 beta mRNA to adjuvant arthritis in the rat. 154 77

Numerous studies have demonstrated the role of the central nervous system in immunomodulation. beta-Endorphin, a neuropeptide that is released along with adrenocorticotropin by the pituitary in response to stress, has been shown to have various effects on immune function, although these effects are dependent on dose, animal model, and immune cell tested. Since the increased risk for infection and tumor that is observed in the elderly is thought to be in part secondary to waning cell-mediated immunity, we investigated the effect of age on beta-endorphin immunomodulation of T-cell proliferation in a murine model. Spleen cells obtained from young and old BALB/c mice were cultured in vitro with various mitogens with and without beta-endorphin. beta-Endorphin at 10(-8) M on day 3 of culture significantly enhanced concanavalin A (2.0 micrograms/10(6) cells per ml) mitogenesis but not phytohemagglutinin or lipopolysaccharide mitogenesis. Moreover, this enhancement was shown only in spleen cells from young mice and was not blocked by the opiate receptor antagonist naloxone, which suggests that enhancement of mitogenesis by beta-endorphin was mediated by a non-opiate receptor. Finally, our results support an altered response to neuroimmunomodulation with age.
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PMID:Aging decreases beta-endorphin enhancement of T-cell mitogenesis in mice. 297 43

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

The plasma concentrations of beta-endorphin was determinated by radioimmunoassay in 75 patients with Wetness-Heat Zheng of Liver and Gallbladder, 23 patients with Insufficient Liver Zheng, 13 patients with Insufficient Spleen Zheng and 30 healthy subjects (control group). Compared with the control group, the plasma beta-EP levels were increased in Wetness-Heat Zheng of Liver and Gallbladder and Insufficient Liver Zheng. The patients with different diseases that were diagnosed to be Wetness-Heat Zheng of Liver and Gallbladder presented high levels of plasma beta-EP. It is suggested that the plasma beta-EP is an important change in the syndrome of Wetness-Heat Zheng of Liver and Gallbladder, and may be used as a diagnostic index.
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PMID:[Clinical study on plasma beta-endorphin levels in patients with wetness-heat zheng of the liver and gallbladder]. 986 16