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)

Rats possess stress-responsive, vasopressin (VP)-expressing and stress-nonresponsive, VP-deficient subpopulations of parvocellular corticotropin-releasing hormone (CRH) neurosecretory cells. Both subpopulations are activated by bacterial lipopolysaccharide (LPS) and cytokines. Lewis rats exhibit hyporesponsive hypothalamo-pituitary-adrenocortical axes (HPAAs). The Lewis CRH neurosecretory system has been reported to be defective in females and normal in males. We used post-embedding electron microscopic (EM) immunocytochemistry to study baseline levels and LPS-stimulated depletion of neurosecretory vesicles. Male Lewis rats possessed normal numbers of CRH+/VP- varicosities and low numbers of CRH+/VP+ varicosities, indicating abnormally low release of VP into portal blood. This defect contrasts with the reported increase in VP content and release in magnocellular neurosecretory cells in Lewis rats.
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PMID:Decreased vasopressin content in parvocellular CRH neurosecretory system of Lewis rats. 781 36

The administration of lipopolysaccharide (LPS) results in the activation of the hypothalamic-pituitary-adrenal axis (HPAA). We recently reported that the participation and interaction of LPS-induced proinflammatory cytokines were obligatory for the stimulation of adrenocorticotropic hormone (ACTH) release by LPS. LPS and LPS-derived cytokines also stimulate the release of histamine (HA). HA is a known hypothalamic neurotransmitter and activates the HPAA. Therefore, to elucidate the role of HA in LPS- and cytokine-induced ACTH release, we evaluated the effects of several HA H1 and H2 receptor antagonists on the ACTH response to LPS, recombinant human interleukin-1 alpha (rhIL-1 alpha) and HA in mice. Although all 3 of the H1 receptor antagonists administered (mepyramine (MEP), diphenhydramine (DPH) or promethazine (PMZ) were able to block the 10-min ACTH response to HA, only PMZ (a less selective H1 receptor antagonist than MEP) was able to reduce the LPS- or rhIL-1 alpha-induced ACTH responses. Ranitidine, a powerful and selective H2 receptor antagonist, had little effect on the LPS- and rhIL-1 alpha-induced ACTH responses, while metiamide (MET), a much less potent first-generation H2 receptor antagonist, substantially diminished ACTH release. The greater effectiveness of PMZ, in contrast to MEP or DPH, probably relates to the ability of phenothiazine derivatives to inhibit non-HA-dependent pathways involved in the stimulation of the HPAA by cytokines; the same may be true of MET.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Systemically administered histamine H1 and H2 receptor antagonists do not block the ACTH response to bacterial lipopolysaccharide and interleukin-1. 782 83

In previous studies, rat adrenal zona glomerulosa (ZG) cells were demonstrated to release interleukin-6 (IL-6). In the current study, cultures of ZG cells and bioassays for tumor necrosis factor (TNF) and IL-6 were used to determine if ZG cells release TNF and to define more fully the factors that regulate ZG IL-6 release. ZG cells released IL-6 and TNF, and this release was stimulated by lipopolysaccharide, interleukin-1 alpha, interleukin-1 beta, a protein kinase C activator, and a calcium ionophore without affecting intracellular adenosine 3', 5'-cyclic monophosphate (cAMP) content. In contrast, adrenocorticotropic hormone (ACTH) increased the intracellular cAMP content, increased basal and secretagogue-stimulated IL-6 release but decreased basal and secretagogue-stimulated TNF release. The effects of ACTH on IL-6 and TNF release may be mediated by increases in intracellular cAMP because ACTH and dibutyryl cAMP modified IL-6 and TNF release in an identical manner. Therefore, IL-6 and TNF release from ZG cells can be differentially regulated. Because IL-6 and TNF modify adrenal steroid release, the adrenal production of these cytokines may have a role in the stress response.
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PMID:Differential release of tumor necrosis factor and IL-6 from adrenal zona glomerulosa cells in vitro. 784 Jan 68

A complete regulatory loop exists between the immune and neuroendocrine systems. Proinflammatory mediators such as endotoxin (lipopolysaccharide) and interleukin-1 (IL-1) are capable of activating the hypothalamic-pituitary-adrenal (HPA) axis at the hypothalamic level, presumably by inducing the synthesis of prostaglandins. We have recently identified abnormalities in the stress-induced activation of the HPA axis in cholestatic rats. Therefore, in rats with cholestasis due to bile duct resection and sham-resected controls, we studied alterations in proinflammatory mediator-induced activation of the HPA axis and documented the role of alterations in hypothalamic prostaglandin synthesis in these abnormalities. Systemic administration of endotoxin and IL-1 resulted in a significant attenuation of adrenocorticotropic hormone (ACTH) release into plasma in bile duct-resected compared with sham-resected animals. This suppression of endotoxin- or IL-1-induced ACTH release in bile duct-resected rats was associated with a complete absence of IL-1-induced hypothalamic release of prostaglandin E2 (PGE2) in vitro in these animals. In contrast, sham-resected rats exhibited a 70% increase in hypothalamic PGE2 secretion in vitro in response to IL-1. However, bile duct-resected rats exhibited HPA axis activation similar to that of sham-resected animals in response to intracerebroventricularly infused PGE2. Therefore, cholestasis in the rat is associated with an attenuation of central activation of the HPA axis by proinflammatory mediators that appears to be mediated, at least in part, by defective IL-1-induced hypothalamic prostaglandin production.
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PMID:Defective interleukin-1-induced ACTH release in cholestatic rats: impaired hypothalamic PGE2 release. 790 Aug 1

We investigated the effect of several opioid peptides on the activation of murine peritoneal exudate macrophages (M phi) in vitro. M phi were treated with interferon (IFN) as a priming agent and bacterial lipopolysaccharide (LPS) as a triggering agent in the presence or absence of opioid peptides. M phi activation was assessed by their tumoricidal activity. When treatment with IFN and LPS resulted in a high level activation of M phi, dynorphin-A exerted no further enhancing effect. When treatment induced only weak activation, however, dynorphin-A augmented the M phi activation. Leucine-enkephalin, methionine-enkephalin, and also beta-endorphin had augmenting effects. An opioid receptor antagonist, naloxone, reduced the effect of dynorphin-A and beta-endorphin. When M phi were treated sequentially with IFN and LPS, beta-endorphin operated in combination with LPS only. Moreover, beta-endorphin was effective for already activated M phi. These results indicate that opioid peptides act on M phi via classical opioid receptors, and that responsiveness to opioid peptides is induced in the triggering stage of M phi activation.
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PMID:Augmenting effect of opioid peptides on murine macrophage activation. 790 88

We measured iodine-125-labeled recombinant human interleukin-1 alpha (125I-IL-1 alpha) binding in the hippocampus, pituitary, liver, spleen and testis, and plasma adrenocorticotropic hormone (ACTH) and corticosterone levels after i.p. injection of various dose and treatment regimens of the bacterial endotoxin, lipopolysaccharide (LPS). Plasma ACTH and corticosterone levels were significantly increased at 2 h after acute administration of LPS (60 or 300 micrograms/mouse). 125I-IL-1 alpha binding in all peripheral tissues examined was significantly and comparably decreased at 2 h after a single injection of 30 micrograms or 300 micrograms LPS/mouse. On the other hand, 125I-IL-1 alpha binding in hippocampus was significantly decreased only after high dose administration of LPS (300 micrograms/mouse). In order to evaluate if activation of IL-1 in brain resulting in the observed decrease in 125I-IL-1 alpha binding may require more sustained exposure to endotoxin, we compared the effects of a single injection (60 micrograms/mouse) and two injections of LPS (30 micrograms/mouse each at 0 and 12 h). A single injection of LPS (60 micrograms/mouse) decreased 125I-IL-1 alpha binding in the testis but not in the hippocampus, while two LPS injections (30 micrograms/mouse each at 0 and 12 h) caused dramatic reductions in 125I-IL-1 alpha binding in both the hippocampus and testis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of interleukin-1 receptors and hypothalamic-pituitary-adrenal axis by lipopolysaccharide treatment in the mouse. 795 41

This study was carried out to investigate the adrenocorticotropic hormone (ACTH) response in rabbits made febrile by systemic injection of lipopolysaccharide (LPS, Salmonella typhosa endotoxin). Intravenous (i.v.) injection of LPS (0.1 microgram/kg and 1.0 microgram/kg) increased rectal temperature (biphasic fever) and the plasma concentration of ACTH (ACTH response) in a dose-related manner. These responses were suppressed by pretreatment with indomethacin (20 mg/kg, subcutaneously). Intracerebroventricular (i.c.v.) administration of indomethacin (400 micrograms) had no effect on the ACTH response to LPS, although it significantly suppressed febrile response. Small increases in plasma concentration of ACTH and significant fevers followed i.c.v. administration of prostaglandin E2 (2 micrograms) or F2 alpha (2 micrograms). I.v. administration of corticotropin releasing factor (CRF) antagonist [alpha-helical CRF (9-41) (200 micrograms/kg)] partly suppressed the ACTH increase induced in plasma by i.v. LPS. These results suggest that prostaglandins synthesized outside the blood-brain barrier play an important role in the ACTH response and that the mechanism for induction of the ACTH response is not exactly the same as that for the febrile response, although prostaglandins are involved in both responses.
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PMID:Elevation of plasma ACTH concentration in rabbits made febrile by systemic injection of bacterial endotoxin. 795 31

The involvement of hypothalamic histaminergic neurons in the mediation of the ACTH and beta-endorphin (beta-END) response to lipopolysaccharide (LPS) endotoxin was investigated in conscious male rats. LPS stimulated the release of ACTH and beta-END dose-dependently and increased the hypothalamic concentration of the histamine (HA) metabolite tele-methylhistamine significantly and that of HA slightly, indicating an increased turnover of neuronal HA. Pretreatment with the HA synthesis inhibitor alpha-fluoromethyl-histidine administered intracerebroventricularly (i.c.v.) or intraperitoneally (i.p.) inhibited the ACTH and beta-END response to LPS about 60%, whereas i.p. administration of the H3 receptor agonist R(alpha)methylHA, which inhibits HA synthesis and release, decreased the response about 50%. Pretreatment with the H1 receptor antagonist mepyramine (67 micrograms x 2 i.c.v.) inhibited the hormone response to LPS about 50%, while pretreatment with equimolar doses of the H2 receptor antagonists cimetidine (67 micrograms x 2 i.c.v.) or ranitidine (83 micrograms x 2 i.c.v.) had no effect on the LPS-induced release of ACTH and beta-END. When the H1 receptor antagonists mepyramine and cetirizine were administered i.p. in doses (10 mg/kg) which penetrate the blood-brain barrier the hormone response to LPS was inhibited 50% and 30%, respectively. Administered i.p. the H2 receptor antagonists had no effect on the hormone response to LPS. We conclude that hypothalamic histaminergic neurons in rats are involved in the mediation of the ACTH and beta-END response to LPS stimulation via activation of central postsynaptic H1 receptors.
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PMID:Role of hypothalamic histaminergic neurons in mediation of ACTH and beta-endorphin responses to LPS endotoxin in vivo. 796 82

The ability of human lymphocytes and mouse splenocytes to secrete corticotropin-releasing factor (CRF) in response to hyperthermia, hyperosmolarity and hypoxia has been shown. Both human T- and B-lymphocytes appear to have this ability. E. coli lipopolysaccharide and concanavalin A can stimulate CRF secretion by B- and T-lymphocytes, respectively, whereas hydrocortisone inhibits the CRF secretion induced by any agent tested. Adrenocorticotropic hormone (ACTH) secretion in response to hyperthermia, hyperosmolarity and hypoxia was demonstrated also, and this secretion could be inhibited by anti-CRF antibodies and by hydrocortisone. We demonstrate that CRF could provide a necessary link between external stimuli such as cellular stress factors and ACTH secretion by immunocytes leading to corticosteroid production and, subsequently, to non-specific defence reaction of the organism. We also describe a model designed to explain the results obtained.
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PMID:Secretion of immunoreactive corticotropin releasing factor and adrenocorticotropic hormone by T- and B-lymphocytes in response to cellular stress factors. 798 May 49

The experiments reported here investigate the conditionability, using taste aversion conditioning, of the antagonistic effects of alpha-MSH on the thermoregulatory changes associated with injection of bacterial endotoxin lipopolysaccharide (LPS) in rats. Animals were administered LPS and then given alpha-MSH, as an unconditioned stimulus (UCS), in association with the novel taste of saccharin, the conditioned stimulus (CS). The temperature response at this time in alpha-MSH-treated rats was similar to that observed in control animals. However, 7 days later, when these animals were again injected with LPS but re-exposed to saccharin alone, there was a significant reduction in the temperature response profile compared to controls. These results demonstrate that in male rats the conditioned antipyretic effect following conditioning with alpha-MSH as the UCS is sufficiently robust to counteract the acute effects on body temperature of an LPS injection at the time of CS reexposure. This complements previous experiments demonstrating that thermoregulation may be influenced by cognitive association.
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PMID:Inhibition of endotoxin-induced temperature change by behavioral conditioning using alpha-melanocyte-stimulating hormone as an unconditioned stimulus. 801 70


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