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 bilateral communication between the immune and neuroendocrine systems plays an essential role in modulating the adequate response of the hypothalamic-pituitary-adrenal (HPA) axis to the stimulatory influence of interleukins (ILs). It is thus reasonable to assume that inappropriate responses of the HPA axis to ILs might play a role in modulating the onset of pathological conditions such as infections. As part of our programme aimed at investigating the ability of ILs to release pro-opiomelanocortin-like peptides and corticosterone in rats exposed to alcohol, we observed that this stimulatory action appeared to be influenced by the gender of the animals. We therefore examined the ability of IL-1 beta, injected peripherally, to stimulate the HPA axis as a function of stage of sexual maturation and the presence or absence of circulating sex steroids. In immature (21 to 22-day-old) rats, both males and females responded to the i.p. administration of 0.5 or 2.0 micrograms IL-1 beta/kg with statistically comparable increases in plasma ACTH levels. In contrast, females released significantly (P < 0.01) more corticosterone in response to the lower dose of cytokine. Forty-day-old intact animals showed no sexual dimorphism in ACTH secretion, but the females again secreted significantly (P < 0.05-0.01) more corticosterone. Gonadectomy, performed 7-8 days prior to the assay, increased the absolute amount of corticosterone released over a 60-min period. A noticeable dimorphism of the ACTH response to IL-1 beta became apparent in 70-day-old intact rats, with females secreting more ACTH than males.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stimulatory effect of interleukin-1 beta on the hypothalamic-pituitary-adrenal axis of the rat: influence of age, gender and circulating sex steroids. 818 63

Immune and neuroendocrine systems interact at various levels. In particular, either cytokines activate the hypothalamus-pituitary-adrenal axis (HPA) or corticotropin-releasing hormone (CRH) induces the release of beta-endorphin from peripheral human mononuclear cells. The aim of the present study was to investigate whether CRH may affect cytokine production and activity in human peripheral blood mononuclear cells (PBMC). Primary cultures of human PBMC and monocytes were used. They were incubated in presence of different doses of synthetic human CRH. Media were collected and interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) levels were measured by ELISA, while interferon-gamma (IFN-gamma) levels were measured by bioassay. In addition, phytohemoagglutinin-induced lymphocyte proliferation was evaluated by testing [3H]thymidine incorporation in the presence of various doses of CRH. CRH significantly increased IL-6 release from PBMC (p < 0.01). The addition of CRH to PBMC significantly decreased IFN-gamma levels, in a dose dependent manner (p < 0.01). No significant effect of CRH was observed on lymphocyte proliferation or IL-1 beta production. The present results suggest a role for CRH as a paracrine mediator for human immune cells, increasing the evidence of a clear correlation between immune and neuroendocrine system.
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PMID:Corticotropin-releasing hormone modulates cytokines release in cultured human peripheral blood mononuclear cells. 824 69

To determine whether interleukin-1 beta (IL-1 beta) in the brain may modulate nociception, recombinant human IL-1 beta (rhIL-1 beta) (1 pg/kg to 1 microgram/kg) was microinjected into the lateral cerebral ventricle of rats and the latency before initiating the licking of their hindpaws after being placed on a hot plate (50.0 +/- 0.1 degrees C) was measured. A significant reduction of the paw-lick latency was observed after injections of nonpyrogenic doses (10 pg/kg to 1 ng/kg) of rhIL-1 beta, showing a maximal response at a dose of 100 pg/kg which began to appear 5 min after injection, reached a peak within 30 min and then gradually subsided. An increase in the amount of rhIL-1 beta to > 1 ng/kg (up to 1 microgram/kg) had no effect on the nociceptive threshold. The rhIL-1 beta-induced hyperalgesia was completely abolished by pretreatment with an IL-1 receptor antagonist (IL-1ra) or Na salicylate. Similar pretreatment with alpha-melanocyte-stimulating hormone (alpha-MSH) also inhibited the rhIL-1 beta-induced hyperalgesia. However, pretreatment with alpha-helical corticotropin-releasing factor (CRF)9-41 failed to affect it. The results suggest that IL-1 beta in the brain produces hyperalgesia by its receptor-mediated and prostaglandin-dependent action which is sensitive to alpha-MSH. The hyperalgesic action of central IL-1 does not appear to depend on the CRF system.
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PMID:Intracerebroventricular injection of interleukin-1 beta induces hyperalgesia in rats. 825 17

The functional relationship between the immune and the hypothalamic-pituitary-adrenal (HPA) axis [and in particular the release of pro-opiomelanocortin (POMC)-related peptides and corticosteroids induced by interleukins (ILs)] is essential for coordinating the appropriate immune responses to pathogens. Exposure of pregnant mammalian females to alcohol results in abnormal immune functions in the offspring, as well as in altered HPA axis activity. We therefore tested the hypothesis that prenatal alcohol exposure might modify the stimulatory action of ILs on the HPA axis of the pups, thus providing a mechanisms through which this treatment results in increased rate of infectious or inflammatory processes. Pregnant dams were fed a liquid alcohol diet throughout gestation. Dams with free access to food (ad libitum group), or dams fed an isocaloric diet in which sucrose replaced alcohol (pair-feeding), were also included. At 22-24 days of age, the pups were injected intraperitoneally with IL-1 beta, corticotropin-releasing factor (CRF), or the vehicle. Blood samples obtained 1-2 hr later indicated that the alcohol diet resulted in significantly blunted adrenocorticotropic hormone (ACTH) and beta-endorphin, but not corticosterone release, in response to IL-1 beta. Pair-fed pups also showed some decrease in their pituitary response, although to a lesser degree. In contrast, there was no measurable difference in the ability of CRF to increase plasma ACTH levels. These results suggest that prenatal exposure to alcohol interferes with the stimulatory action of IL-1 beta on the secretion of POMC-related peptides, a phenomenon probably not caused by decreased pituitary responsiveness to CRF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prenatal alcohol exposure blunts interleukin-1-induced ACTH and beta-endorphin secretion by immature rats. 827 78

Possible interactions between alcohol (EtOH) and interleukins (ILs) were studied in intact and adrenalectomized (ADX) rats. In intact animals, administration of 0.3 or 0.65 g EtOH/kg 30 min to 4 hr earlier did not cause measurable changes in plasma adrenocorticotropic hormone (ACTH) levels measured immediately before acute intravenous injection of IL-1 beta or endotoxin [lipopolysaccharide (LPS)], and did not interfere with the ability of either treatments to increase ACTH secretion. Administration of 1.5 g EtOH/kg, on the other hand, resulted in elevated plasma ACTH and corticosterone 30 min later, and significantly decreased the magnitude of the ACTH response to IL-1 beta in both intact and ADX rats. When administered 4 hr before the cytokine, however, 1.5 g EtOH/kg did not alter the responsiveness of the hypothalamic-pituitary-adrenal (HPA) axis to IL-1 beta. Studies of the reverse paradigm were conducted in rats injected with LPS, a means of increasing endogenous IL-1 levels. Intraperitoneal administration of alcohol 4 hr later resulted in measurably blunted ACTH release by intact rats, but not ADX animals. We conclude that when prior alcohol administration does not result in elevated ACTH levels at the time of IL-1 injection, no alteration in the HPA axis' response to the cytokine is observed. As we have shown in other experiments that circulating levels of corticosterone were temporarily increased by all doses of alcohol used in the present study, these results suggest that steroid feedback did not play a major role in modulating the ability of IL-1 beta to activate the HPA axis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute interactions between cytokines and alcohol on ACTH and corticosterone secretion in the rat. 827 79

The susceptibility of Lewis rats is related to blunted hypothalamic-pituitary-adrenal (HPA) axis responsiveness to a variety of inflammatory and neuroendocrine stimuli. In contrast resistance to inflammatory disease of histocompatible Fischer rats is associated with their intact HPA axis responses to the same stimuli. We have examined the contribution of IL-1 beta to in vitro corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) release from hypothalamic explants derived from LEW/N and F344/N rats. The same animal model has been used to investigate the regulatory effect of alpha MSH, an immunosuppressive neurohormone, on IL-1 beta stimulated CRH and AVP secretion. CRH basal release in both strains was similar. However, LEW/N hypothalamic AVP basal secretion was significantly elevated. CRH relative response of LEW/N hypothalamic explants to IL-1 beta stimulation was lower compared to Fischer, which is consistent with their hyporesponsiveness to inflammatory mediators. AVP secretion however, was significantly decreased in hypothalamic explants from both strains after 40 min exposure to IL-1 beta. alpha MSH suppressed basal CRH and AVP release in both LEW/N and F344/N rats and prevented IL-1 beta stimulated CRH secretion in these strains. AVP was further diminished in F344/N explants following incubation with alpha MSH + IL-1 beta, while LEW/N level was significantly elevated. However, AVP levels remained significantly below baseline in explants from both strains after final incubation with IL-1 beta. Although our findings indicate a modulatory action of alpha MSH in HPA axis regulation in vitro, the physiological importance of this phenomenon in Lewis and Fischer rats requires further investigation.
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PMID:Release of hypothalamic corticotropin-releasing hormone and arginine-vasopressin by interleukin 1 beta and alpha MSH: studies in rats with different susceptibility to inflammatory disease. 829 92

A large body of recent evidence suggests that a number of inhibitory and excitatory neuropeptides and amino acids may participate in the episodic secretion of hypothalamic LHRH and pituitary LH in castrated rats. However, the precise functional relationships among these messenger molecules in the control of LH secretion remain to be ascertained. The aim of this study was to test the hypothesis that inhibition of LH release by an opioid [beta-endorphin (beta END)], cytokine [interleukin-1 beta (IL-1 beta)], or tachykinin [neuropeptide-K (NPK)] is a result of diminished excitatory amino acid (EAA) signaling. Adult male rats were castrated and received an intracerebroventricular cannula in the third ventricle for administration of beta END (10 micrograms/rat), NPK (2.5 nmol/rat), or IL-1 beta (100 ng/rat) 2 weeks postcastration. One day before the experiments, rats received an intraatrial cannula for frequent blood sampling and for iv injection of the glutamate receptor agonist N-methyl-D-aspartate (NMDA; 5 mg/kg) at 30-min intervals. Blood samples for LH measurements were withdrawn immediately before and 10 min after each NMDA injection. The results show that intracerebroventricular beta END, IL-1 beta, or NPK inhibited LH release. Multiple injections of NMDA did not alter the existing pattern of LH secretion in castrated control rats. However, similar NMDA injections completely prevented the decrease in LH release by beta END, IL-1 beta, or NPK. Plasma LH levels in these rats remained within the range seen in untreated control rats throughout the 120-min duration of the experiment, and NMDA injections at 30-min intervals evoked pulses of LH that resembled those seen normally in castrated rats. The blockade of the inhibitory effects of the three peptides by NMDA and previous knowledge of hypothalamic sites of NMDA action suggest that EAA systems may represent a common pathway down-stream in the hypothalamic LHRH-regulating circuitry to mediate diminution of LH release by inhibitory peptides. Further, their inhibitory influence may be exerted either directly at the level of LHRH neurons and/or by diminution in EAA efflux, leading to suppression of LHRH and LH release.
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PMID:Evidence that luteinizing hormone suppression in response to inhibitory neuropeptides, beta-endorphin, interleukin-1 beta, and neuropeptide-K, may involve excitatory amino acids. 831 64

alpha-Melanocyte-stimulating hormone (alpha-MSH), adrenocorticotrophic hormone (ACTH), beta-endorphin, cortisol, and the cytokines interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF alpha) were measured in 80 AIDS patients (group IV CDC) and in healthy hospital personnel. The average plasma alpha-MSH was significantly greater in AIDS patients than in control subjects; no significant differences between groups were observed in the average concentrations of ACTH, cortisol, and beta-endorphin; plasma cytokines were likewise similar in the two groups. Plasma concentrations of alpha-MSH and ACTH were inversely related in AIDS patients and a similar inverse relation between alpha-MSH and IL-6 was also observed in these patients. There were positive relations among elevated circulating ACTH, cortisol, IL-6, and high fever in AIDS patients with severe concomitant disease. Plasma alpha-MSH concentrations within a specific range correlated positively with 6 month survival. Because cytokines can stimulate HIV expression in certain cell types and they are believed to have a role in disease progression in HIV-infected patients, it may be that a potent endogenous modulator of cytokine action such as alpha-MSH is crucial to survival in these patients.
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PMID:Proopiomelanocortin-derived peptides and cytokines: relations in patients with acquired immunodeficiency syndrome. 838 70

Numerous reports have demonstrated that interleukin-1 beta (IL-1 beta) is a potent secretagogue for adrenocorticotropin (ACTH) and that IL-1 alpha appears to be considerably less efficacious. To clarify apparent differences in the potency of IL-1 alpha vs. -beta on ACTH secretion from a functional perspective, the IL-1 receptor antagonist protein, IRAP, was utilized. Following administration to rats either intravenously (i.v.) or adjacent to the median eminence (intra-ME), IL-1 beta was approximately 8-fold more potent than IL-1 alpha. IRAP, delivered i.v. or intra-ME, inhibited ACTH secretion due to the administration of IL-1 alpha or -beta by the corresponding route. Similar amounts of IRAP were required to attenuate ACTH responses to approximately equieffective i.v. doses of IL-1 alpha (200 ng) or -beta (25 ng): IC50 for IRAP inhibition of IL-1 alpha vs. -beta was approximately 2.5 or 5.5 micrograms, respectively. At these IC50 doses, the ratios of IRAP/IL-1 were 12.5 and 220 for IL-1 alpha vs. -beta, respectively. These ratios are compatible with mediation by a type I-like IL-1 receptor. To compare these properties of the central IL-1 receptor to a peripheral type I IL-1 receptor in the same species, the IL-1-enhanced rat thymocyte comitogenesis assay was utilized. Thymocyte proliferation in response to equieffective doses of IL-1 alpha or -beta was similarly inhibited by IRAP:approximate IC50 for inhibition of IL-1 alpha vs. -beta was 12.5 or 25 ng/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interleukin-1 alpha and interleukin-1 beta stimulate adrenocorticotropin secretion in the rat through a similar hypothalamic receptor(s): effects of interleukin-1 receptor antagonist protein. 838 18

Neutrophil (PMN) accumulation induced by interleukin-1 beta (IL-1 beta, 5-20 ng) into the mouse air pouch was inhibited in a dose-dependent manner (2-200 micrograms) by concomitant injection of IL-1 receptor antagonist (IL-1RA). Similarly, co-administration of the neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) resulted in a reduction of the number of migrated PMN but only at the highest dose tested (200 micrograms). Although IL-1RA does not select between the two types of receptors so far described for IL-1, the effectiveness of alpha-MSH suggests that this property of the cytokine may occur through IL-1 type I receptor. This observation was confirmed by using a specific monoclonal antibody (mAb) raised against this receptor type, and which strongly inhibited (87%) IL-1-induced PMN recruitment.
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PMID:Pharmacology of interleukin-1-induced neutrophil migration. 839 Dec 1


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