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 present study compares the effects of endotoxin, a key factor in gram-negative bacterial infection, and of corticotropin-releasing hormone (CRH) on ACTH and cortisol secretion in healthy male volunteers in a placebo-controlled design. Endotoxin (isolated from Salmonella abortus equi; 0.4 ng/kg body weight) induced a significantly delayed and prolonged increase of ACTH and cortisol secretion as compared to CRH (100 micrograms), supporting the hypothesis that different intermediate mechanisms are involved (baseline/peak: ACTHEndotoxin vs. ACTHCRH: 140 +/- 40 min vs. 44 +/- 17 min (p < 0.001); CortisolEndotoxin vs. CortisolCRH: 113 +/- 51 min vs. 66 +/- 31 min (p < 0.05); peak/baseline: ACTHEndotoxin vs. ACTHCRH: 244 +/- 79 min vs. 200 +/- 25 min (p < 0.05); CortisolEndotoxin vs. CortisolCRH: 278 +/- 76 min vs. 182 +/- 16 min (p < 0.001)). Activation of the hypothalamo-pituitary-adrenocortical (HPA) system by endotoxin in men is associated with increased interleukin-6 (peak value: 124 +/- 109 pg/ml) and tumor necrosis factor-alpha (peak value: 69 +/- 53 pg/ml) plasma levels which, probably together with locally produced interleukin-1, stimulate the HPA system both at the hypothalamic and (to a lesser degree) at the pituitary site. Provided that strictly controlled laboratory conditions are applied, the endotoxin challenge test presented here may serve as an appropriate and safe tool to explore an individual's capacity for neuroendocrine adaptation to a bacterial stressor, thus providing information complementary to the CRH test.
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PMID:Endotoxin- and corticotropin-releasing hormone-induced release of ACTH and cortisol. A comparative study in men. 826 45

Cytokines, which include interferons (IFNs), interleukins (ILs), and tumor necrosis factor (TNF), are immunoregulatory proteins produced by lymphocytes and inflammatory cells. Several cytokines, most noteworthy IFNs and ILs, stimulate glucocorticoid secretion. In this study, the effects of variable doses and repetitive administration of IFNs and TNF on secretion of pituitary hormones and cortisol were measured. Patients were given for a period of 15 days on alternating days injections of IFN-beta (IFN-beta ser), 90 or 450 x 10(6) IU, IFN-gamma, 0.1-100 x 10(6) IU, or TNF 125-275 micrograms/m2. Sixty to 120 min after IFN-beta ser injection median levels of cortisol, adrenocorticotropin (ACTH), prolactin (PRL), and growth hormone (GH) rose two-fold. Urinary free cortisol excretion increased significantly during the day following IFN-beta ser administration. IFN-gamma > or = 30 x 10(6) IU caused a comparable rise in plasma cortisol. TNF induced two- to four-fold increases in ACTH and cortisol. The fact that increased cortisol secretion was associated with a rise in the level of ACTH as well as PRL and GH suggests that the cytokines increased cortisol by stimulating the anterior pituitary. The hormonal response induced by cytokines was unrelated to their pyrogenic effect, undiminished with repetitive treatment, and not dose-dependent above a threshold level. These observations reinforce the concept of a physiologic link between the immune system and the hypothalamic-pituitary-adrenal (HPA) axis.
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PMID:Effects of cytokines on the pituitary-adrenal axis in cancer patients. 830 Nov 55

A panel of long-term murine T lymphocyte clones specific for the glycoprotein of vesicular stomatitis virus (VSV) in association with either H-2I-Ad or I-E(d) was tested for the production of cytokines in both resting and poststimulation states using both in situ hybridization and bioassay. All but one of the clones showed antigen-specific cytolytic activity in a 4-hr 51Cr release assay. Unexpectedly, the clones did not appear to be typical Th1 cells. Five of these T cell clones produced both IL-2 and IFN-gamma but not IL-4 after stimulation with either phorbol 12-myristate 13-acetate (PMA) or concanavalin A (Con A). Some clones constitutively expressed mRNA for IL-2 and INF-gamma. The proliferation of these clones was factor independent, suggesting an autocrine growth mechanism. Three clones produced variable levels of IL-4 mRNA and some, to significant quantities, of IL-2 mRNA. One cytolytic clone produced neither IL-2 nor IL-4 mRNA to detectable levels, although mRNA for IFN-gamma was observed. A noncytolytic, Ag-specific clone produced IL-6, tumor necrosis factor (TNF), and lymphotoxin (LT), but no IL-2, IL-4, or IFN-gamma mRNA. There was a strong quantitative correlation between the expression of IL-2-, INF-gamma-, and LT-specific mRNAs by the clones. All the T cell clones tested which secreted INF-gamma and LT expressed no measurable IL-4 mRNA. We examined expression of several other genes in the panel of clones. These included TNF, met-enkephalin (met-enk), IL-1, and IL-6. IL-1 m-RNA synthesis was not observed in any of the T cell clones. Almost all clones produced TNF mRNA. Parallel bioassays showed that secreted IL-2/IL-4 activity levels and mRNA levels correlated well for all clones. Thus, we observed a great degree of heterogeneity among CD4+ cytolytic T lymphocyte clones.
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PMID:Lymphokine expression profile of resting and stimulated CD4+ CTL clones specific for the glycoprotein of vesicular stomatitis virus. 838 Oct 52

Insulin-like growth factor-II (IGF-II) gene expression is induced by adrenocorticotropic hormone (ACTH) in human fetal adrenals (HFA), which suggests an important role for IGF-II in HFA growth and differentiation. Many cytokines have different regulatory actions in the endocrine glands. In the present study we have investigated the effects of two cytokines, tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), on the regulation of IGF-II gene expression in cultured HFA cells. Both TNF-alpha and IFN-gamma inhibited basal and ACTH-induced accumulation of IGF-II mRNA dose-dependently. Cell viability was not altered by treatment with TNF-alpha or IFN-gamma. In addition, the combination of TNF-alpha and IFN-gamma decreased ACTH-induced IGF-II mRNAs more potently than each cytokine alone. Our results suggest that TNF-alpha and IFN-gamma may be involved in the regulation of HFA growth and differentiation via local IGF-II production.
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PMID:Tumor necrosis factor-alpha and interferon-gamma inhibit insulin-like growth factor II gene expression in human fetal adrenal cell cultures. 838 14

Opioid peptides activate immunocytes and opiate alkaloids inhibit this activation in the mussel, Mytilus edulis. Here we present evidence that cells of another invertebrate, Leucophaea maderae, can be influenced in a similar way by the Met-enkephalin analogue D-Ala2-Met5-enkephalin (DAMA) and morphine. Effects of different signal molecules on Leucophaea hemocytes were evaluated by computer-assisted image analysis of their conformational state. A small percentage of the untreated cells were found to display spontaneous conformational changes after 25 min of incubation without pharmacological agents which was noted as a decrease in both circularity factor and shape factor values. Activation caused the cells to become elliptical, a feature that appears to be characteristic of Leucophaea immunocytes. Administration of DAMA induced a similar activation of most of the cells. After 30 min these DAMA-activated cells started to display distinct locomotory activity not seen in the controls. alpha-Melanocyte-stimulating hormone (MSH, 10(-7)) added to the incubation medium after DAMA-activation caused the cells to return to their original "rounded" conformation. In addition, the presence of immunoreactive interleukin (IL-1), adrenocorticotropin (ACTH) and tumor necrosis factor (TNF) in the hemolymph was demonstrated. These data suggest an interaction between both vertebrate-type immunological signal molecules and neuropeptides in the regulation of immunological cells in Leucophaea.
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PMID:The presence and effects of mammalian signal molecules in immunocytes of the insect Leucophaea maderae. 858 63

alpha-Melanocyte-stimulating hormone (alpha-MSH), a tridecapeptide derived from pro-opiomelanocortin, has potent antiinflammatory activity in laboratory animals. alpha-MSH inhibits nitric oxide production by murine macrophages, an influence believed to reflect activation of an autocrine circuit in these cells, one that is based on production and release of alpha-MSH and subsequent stimulation of melanocortin receptors. We found that THP-1 cells, human monocytic cells, produced alpha-MSH; this production was increased by interleukin-6, tumor necrosis factor a, or concanavalin A. These cells also expressed the gene for the human alpha-MSH receptor MC1. Unlike murine macrophages, THP-1 cells produced little nitrite in response to interferon-gamma (IFN-gamma) and lipopolysaccharide, and a-MSH inhibited this production only slightly. However, production of neopterin, a presumed primate homologue of nitric oxide in lower animals, was increased in THP-1 cells stimulated with INF-gamma plus TNF-alpha and alpha-MSH significantly inhibited this production. The evidence indicates that an autocrine regulatory circuit based on alpha-MSH occurs in human monocyte/macrophages much as in murine macrophages. alpha-MSH-induced modulation of specific inflammatory mediators/cytotoxic agents appears to differ depending on the importance of the mediators in the myelomonocytic cells of different species.
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PMID:alpha-MSH production, receptors, and influence on neopterin in a human monocyte/macrophage cell line. 860 97

We examined whether arginine vasopressin (AVP) is involved in the adrenocorticotropin (ACTH) response induced by interleukin (IL)-6 or tumor necrosis factor (TNF)-alpha in the rat. To accomplish this, we employed immunoneutralization of brain AVP by injecting anti-AVP antiserum intracerebroventricularly (i.c.v., 3rd ventricle). For comparison, we also tested the effect of immunoneutralization of corticotropin-releasing hormone (CRH) in the brain. Anti-CRH antibody, anti-AVP antibody, or normal rabbit serum (control) was given i.c.v. 15 min before an i.c.v. administration of human recombinant IL-6 (100 ng) or TNF-alpha (100 ng). Both IL-6 and TNF-alpha significantly elevated plasma ACTH levels. The IL-6-induced ACTH response was significantly suppressed by both anti-CRH and anti-AVP antibodies. On the other hand, the TNF-alpha-induced ACTH response was not significantly affected by anti-AVP antibody, although anti-CRH antibody could suppress the response. These results suggest that the IL-6-induced ACTH response may be mediated by both CRH and AVP, whereas the ACTH response to TNF-alpha is only via CRH.
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PMID:In vivo evidence that arginine vasopressin is involved in the adrenocorticotropin response induced by interleukin-6 but not by tumor necrosis factor-alpha in the rat. 864 62

Interleukin 6 (IL-6) and tumor necrosis factor (TNF) are released from the zona glomerulosa of rat adrenal glands. The release of these cytokines from adrenal cells is regulated by interleukin 1 beta (IL-1 beta) and lipopolysaccharide (LPS), which are involved in the immune and inflammatory responses. Adrenocorticotropic hormone (ACTH) and angiotensin II, hormones that regulate the adrenal cortex, likewise regulate release of cytokines from adrenal glands. Dopamine inhibits aldosterone release from the adrenal cortex. Therefore, effects of dopamine on IL-6 and TNF release from rat adrenal zona glomerulosa were investigated. Primary cultures of rat adrenal zona glomerulosa cells were exposed to test agents and IL-6 and TNF release determined by the 7TD1 and WEHI bioassays, respectively. Dopamine increased basal IL-6 release and potentiated IL-6 release stimulated by ACTH, LPS or IL-1 beta. Dopamine inhibited basal and secretagogue-stimulated (LPS and IL-1 beta) TNF release. These effects of dopamine were mediated by D2 receptors because N-0437, a D2 agonist, had effects on TNF and IL-6 release identical to those of dopamine. Therefore, dopamine, through D2 receptors, regulates the release of IL-6 and TNF from adrenal cells. Because TNF and IL-6 regulate adrenal steroid release, these cytokines may serve as autocrine or paracrine mediators of adrenal gland function.
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PMID:Dopamine increases interleukin 6 release and inhibits tumor necrosis factor release from rat adrenal zona glomerulosa cells in vitro. 866 82

The neuropeptide alpha-melanocyte stimulating hormone (alpha-MSH), a proopiomelanocortin derivative, is a potent modulator of fever, inflammation, and other aspects of the acute-phase response. Alpha-MSH concentrations increase in rabbit plasma after large doses of endotoxin, but it is not known if changes in this potent peptide likewise occur during endotoxemia in humans. The current study performed to assess changes in plasma alpha-MSH during the acute inflammatory response to endotoxin in normal humans. Alpha-MSH was measured in plasma samples obtained over a 5-hour study period in 20 normal human subjects given endotoxin. Plasma adrenocorticotropic hormone (ACTH) and tumor necrosis factor were also measured at the same time points. Endotoxin administration caused fever-related increases in plasma alpha-MSH. Five subjects with a high thermal response to endotoxin (> 2.6 degrees C above baseline) showed a 2- to 4-fold increase in circulating alpha-MSH whereas subjects with low fever (< 2.3 degrees C) did not. Tumor necrosis factor was detected in all subjects after endotoxin, but its peak was significantly less (p < 0.01) in those subjects who had substantial increases in alpha-MSH. Plasma ACTH increased in all subjects given endotoxin, but unlike its 1-13 derivative alpha-MSH, the increases were not commensurate with fever. The data show that challenge with endotoxin causes alpha-MSH release in normal human subjects with high fever. The positive relationship between increases in circulating alpha-MSH and high thermal response together with previous evidence from animal studies suggest that the neuropeptide is an endogenous modulator of host responses.
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PMID:Endotoxin causes release of alpha-melanocyte-stimulating hormone in normal human subjects. 873 98

Cytokines are soluble mediators of immune function that also regulate several endocrine systems. Interleukin-1 (IL-1), IL-6 and tumor necrosis factor-alpha (TNF alpha) each mediate certain aspects of inflammation. In addition, these agents regulate hormone secretion from and cellular proliferation within endocrine tissues. Thus, IL-1 and IL-6 each affect hormone release from anterior pituitary cells (e.g., growth hormone) and inhibit the proliferation of these cells. Cytokines are also localized within discrete nuclei of the hypothalamus (e.g., IL-1 in the paraventricular nucleus), where they may affect production of neuropeptides and biogenic amines (e.g., corticotropin-releasing hormone). Similarly, IL-1 and TNF alpha affect granulosa cell steroidogenesis and IL-6 production. Follicular atresia may either be augmented or inhibited by cytokines depending on their ability to regulate cellular apoptosis. Compartmentation of cytokines within adrenal tissue (e.g., IL-6 in the zona glomerulosa) allows localized effects of these factors on glucocorticoid secretion. Thus, cytokines affect via paracrine or autocrine pathways both hormone secretion from, and possibly cellular differentiation within, endocrine tissues.
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PMID:Role of the cytokines in the hypothalamic-pituitary-adrenal and gonadal axes. 873 3


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