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)

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

To study the effects of the cytokine and neuroendocrine hormone beta-endorphin on the transendothelial migration of neutrophils, bovine pulmonary artery endothelial cells were grown to confluence on PVP-free polycarbonate filters coated with gelatin. Pretreatment of endothelial cell cultures with 1 to 10 mumol/liter of beta-endorphin for 60 min resulted in significantly stimulated migration of subsequently added neutrophils across the endothelial monolayer. The number of neutrophils that migrated across beta-endorphin-treated endothelial cells was similar to the number that traversed untreated monolayers in response to gradients of formylpeptide. Consistently, an additive effect was seen when migration was induced by both beta-endorphin pretreatment of the endothelial cells and a formylpeptide chemotactic gradient. When used at optimal concentration, beta-endorphin was equally effective in stimulating neutrophil migration as was tumor necrosis factor-alpha. In the absence of formylpeptide the effect of apical surface exposure of endothelial cells to beta-endorphin versus basal surface exposure was comparable. Stimulation of neutrophil transendothelial migration in this system appeared to be specific and mediated by opiate receptors, since excess concentration of naloxone completely abolished the effect of beta-endorphin but not of tumor necrosis factor-alpha. These results suggest that beta-endorphin, released during stress, may act upon the endothelium to promote emigration of neutrophils from the vasculature.
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PMID:Migration of neutrophils across endothelial monolayers is stimulated by treatment of the monolayers with beta-endorphin. 786 98

Various reports have shown that invertebrate hemocytes are responsive to mammalian neuropeptides and cytokines. In the present study, we demonstrate that corticotropin-releasing factor (CRF) and adrenocorticotropin (ACTH) fragments (1-24), (1-4), (4-9), (1-13), (1-17), and (11-24) significantly stimulate molluscan hemocyte migration, and the whole sequence (1-39) and the fragment (4-11) have an inhibitory effect. Differences between species were found with respect to the response to individual fragments. Additionally, the (4-11) fragment was able to antagonize some of the stimulatory fragments (4-9) as well as tumor necrosis factor (TNF-alpha)-induced chemotaxis. Our results suggest that invertebrate hemocytes are able to respond to CRF and ACTH fragments that in turn provide further evidence of the complexity of intercellular signaling within the immune system in relatively primitive animals. Thus, auto- and neuroimmunoregulatory activities in mammals must have had an earlier beginning than previously believed.
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PMID:Differential modulation of invertebrate hemocyte motility by CRF, ACTH, and its fragments. 800 24

Using an antiserum against tumor necrosis factor (TNF)-alpha and an interleukin (IL-1) receptor antagonist, we studied putative roles of these cytokines in mediating the endotoxin-induced elevation of plasma adrenocorticotropic hormone (ACTH) and corticosterone levels in freely moving rats. Intravenous administration of Escherichia coli lipopolysaccharide (LPS) increased plasma ACTH and corticosterone levels in a dose-dependent manner. The plasma corticosterone reached to its highest level among a series of experiments after the administration of even the smallest dose (0.03 microgram/kg) tested. Plasma ACTH and corticosterone levels in these rats were completely inhibited by the intravenous administration of anti-murine TNF-alpha-rabbit antiserum (anti-TNFAS) after the administration of LPS but not by the intravenous administration of IL-1 receptor antagonist (IL-1RA). On the other hand, both recombinant human IL-1RA and anti-TNFAS significantly inhibited plasma ACTH increase stimulated with 10 micrograms/kg LPS. These findings indicate that 1) when the plasma corticosterone increase induced by intravenous LPS remains below its maximum, the effect is exclusively mediated by TNF-alpha, and 2) when a larger amount of LPS is administered, both IL-1 beta and TNF-alpha participate at least in part in the hypothalamic-pituitary-adrenal axis activation.
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PMID:Effect of IL-1 receptor antagonist and antiserum to TNF-alpha on LPS-induced plasma ACTH and corticosterone rise in rats. 802 31

The present study was designed to investigate the coupling mechanisms linking the immune and the neuroendocrine corticotropic systems in an integrated defense response triggered by an infectious aggression. The experimental paradigm used consisted of the exploration in individual conscious rats of the temporal pattern of increased plasma concentrations of the two stress hormones, adrenocorticotropic hormone (ACTH) and corticosterone (Cort), and of three cytokines known as ACTH stimulators, tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta, and IL-6, after intra-arterial infusions of lipopolysaccharide (LPS) given at three doses, 5 micrograms/kg (LPS-5), 25 micrograms/kg (LPS-25), and 1 mg/kg (LPS-1,000). Blood samples were taken 30 min and immediately before LPS injection (t0) and at 15, 30, 60, 120, 300, and 480 min post-LPS. The three doses of LPS induced ACTH and Cort surges, starting after 30 min for LPS-5 and LPS-25 or 15 min for LPS-1,000 and peaking with a similar amplitude at 60 min before receding slowly to baseline at 480 min for the two lower LPS doses. On the other hand, whatever the LPS dose, none of the three cytokines rose above undetectable basal levels before 60 min. They increased thereafter to culminate 10- to 30-fold above baseline at 60 min (TNF-alpha) or 120 min (IL-1 beta and IL-6) after LPS and declined back to basal levels at 300 min (TNF-alpha, all doses, and IL-6 for LPS-5 and LPS-25). After LPS-25, only IL-1 beta had not regressed to baseline levels at 480 min.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Temporal cascade of plasma level surges in ACTH, corticosterone, and cytokines in endotoxin-challenged rats. 804 20

The neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) has potent antipyretic and antiinflammatory properties. When administered systemically, the naturally occurring molecule and its COOH-terminal tripeptide sequence inhibit inflammation induced by peripherally applied irritants and intradermal injections of mediators of inflammation such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF alpha). We recently found that alpha-MSH can act solely within the brain to inhibit inflammation caused by a general irritant applied to the skin. This activity appears to be shared with salicylate drugs and the combined observations suggest the existence of descending neurogenic antiinflammatory signals capable of modulating inflammation in peripheral tissues. To improve our knowledge of the scope of this action of the peptide, alpha-MSH was injected into the cerebral ventricles (i.c.v.) of mice that had received intradermal injections in the ear of mediators of inflammation: IL-1 beta, IL-8, leukotriene B4, and platelet-activating factor. The centrally administered peptide inhibited the actions of all of these proinflammatory agents as determined from comparisons with measures of ear edema over time in control animals; this indicates that the central peptide can alter inflammation induced in the periphery by major mediators of inflammation. In tests confined to IL-1 beta, central administration of alpha-MSH(11-13) was also effective. These findings support the concept of a descending neurogenic antiinflammatory influence promoted by an action of alpha-MSH within the brain, an inhibitory influence that is not restricted to modulation of just one or a limited set of the mediators of inflammation.
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PMID:Central neurogenic antiinflammatory action of alpha-MSH: modulation of peripheral inflammation induced by cytokines and other mediators of inflammation. 812 2

In addition to the magnocellular hypothalamic nuclei, arginine vasopressin (AVP)-containing neurons have also been identified in limbic structures, including the hippocampus and amygdala. In the present study, we compared the qualitative properties of the in vitro release of AVP from the dissected hypothalamus with the in vitro release from the dissected amygdala and used these release systems to evaluate the interactions with neurotransmitters and cytokines. The areas of the paraventricular nucleus and supraoptic nucleus that contain the AVP neurons and that receive cholinergic innervation are also interleukin (IL)-1 beta immunoreactive. Acetylcholine or high KCl (60 mM) induces AVP release in both regions, and the AVP release is calcium dependent. Acetylcholine-induced AVP release is antagonized by atropine or mecamylamine, indicating that both muscarinic and nicotinic receptors are mediating the cholinergic effect in these brain regions. IL-1 beta (100 U/ml) had no effect on the basal AVP release from the hypothalamus, but significantly potentiated the acetylcholine-induced AVP release, lowering the threshold from 500 to 100 nM. This effect was completely blocked in the presence of neutralizing antibodies to IL-1 beta, atropine (10 microM) or mecamylamine (10 microM). IL-6, like IL-1 beta, also potentiated acetylcholine-induced AVP release, but to a lesser extent. Neither tumor necrosis factor-alpha nor interferon-gamma had any effect on the basal or acetylcholine-induced AVP release from the hypothalamus. None of the cytokines tested had any effect on the basal or acetylcholine-induced AVP release from the amygdala. Our results suggest a hypothalamic site of action of IL-1 beta and IL-6 on the acetylcholine-induced AVP release. The stimulatory effects of IL-1 and IL-6 on adrenocorticotropin release have been ascribed to an increased release of corticotropin-releasing factor (CRF). These data further suggest that, in addition to CRF, AVP plays a role in the bidirectional communication between neuroendoc ine and immune systems. Understanding the mode of interaction between IL-1 beta and IL-6 with AVP could clarify pathophysiologic or toxic effects of high brain levels of these cytokines.
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PMID:IL-1 beta potentiates the acetylcholine-induced release of vasopressin from the hypothalamus in vitro, but not from the amygdala. 815 70

Current knowledge about the pathophysiology of septic shock is reviewed, and biotechnology-based therapies under development are discussed. Patients with septic shock begin their clinical course with leukocytosis, fever, tachycardia, tachypnea, and organ hypoperfusion; shock ensues as immunologic and vasoactive mediators produce hypotension. There are many metabolic and cardiovascular responses, and single- or multiple-organ failure is common. Patients may experience adult respiratory distress syndrome. A multitude of endogenous and exogenous factors have been linked to the pathophysiology of sepsis and septic shock, including (1) endotoxin from gram-negative bacteria, (2) peptidoglycan and exotoxins from gram-negative bacteria, (3) endotoxin-binding proteins and receptors, (4) bactericidal proteases, (5) exotoxins from gram-positive bacteria, (6) acute-phase proteins and proteases, (7) cytokines, (8) arachidonic acid metabolites, (9) complement, (10) beta-endorphin, (11) histamine, (12) stimulation of intrinsic and extrinsic coagulation pathways and proteases, and (13) endothelium-derived factors and adhesion molecules. Molecular entities and strategies under development to combat septic shock include monoclonal antibodies to endotoxin, active immunization with lipid-A analogues, bactericidal permeability-increasing protein, interleukin inhibitors, and inhibitors of tumor necrosis factor-alpha. Successful treatment of septic shock will probably require a combination of agents, including antimicrobials. An ideal goal for biotechnology in the area of septic shock is to prevent invading pathogens from overstimulating the host's immune system and to systematically eliminate those pathogens. Biotechnology is opening new avenues to the treatment of septic shock.
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PMID:Pathophysiology of septic shock and implications for therapy. 816 70

Fever is induced by interactions of bacterial pyrogens with cells from the immune system, which subsequently release a cascade of cytokines. After intramuscular injection of lipopolysaccharide (LPS) from E. coli, increased amounts of tumor necrosis factor (TNF) and interleukin-6 (IL-6) can be measured in blood plasma and in perfusates of the anterior hypothalamus, where body temperature is regulated. These substances are therefore candidates to be involved in the modification of thermoregulatory structures leading to the febrile rise in body temperature. This increase of body temperature is limited and sometimes even prevented by the actions of endogenous antipyretic neuropeptides like arginine vasopressin (AVP), adrenocorticotropin (ACTH) and melanocyte-stimulating hormones (MSHs) liberated within the brain or systemically during fever. For AVP, most experimental evidence confirms antipyretic pathways from the hypothalamic paraventricular nucleus to the septal area of the limbic system, which are activated during fever and by several stressful stimuli. Fever and endogenous antipyresis are interconnected and result from interactions between the immune system and the central nervous system.
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PMID:Neurobiological concepts of fever generation and suppression. 825 4

Endotoxin, a potent stimulator of the immune system and an important mediator in the pathophysiology of septic shock, has been shown to alter the release of certain hormones following its systemic administration. The purpose of this study was to determine the effects of endotoxin on pituitary hormone secretion both in vivo and in vitro in sheep, with emphasis placed on its effects on growth hormone (GH) release. Endotoxin (400 ng/kg i.v.) increased plasma GH, adrenocorticotropic hormone (ACTH), cortisol and prolactin, while it decreased luteinizing hormone (LH) pulse frequency (p < 0.05). Plasma levels of tumor necrosis factor, a major mediator of endotoxin effects, also increased following endotoxin administration. Endotoxin did not affect the GH response to human GH-releasing hormone. In vitro studies evaluated the effect of endotoxin to alter GH secretion from dispersed sheep anterior pituitary cells at dosages of 1, 10 and 50 micrograms/ml, with samples collected at 4, 8 and 24 h. Endotoxin increased pituitary GH secretion at 24 h for 1 microgram/ml (p < 0.05) and at all time periods for 10 and 50 micrograms/ml (p < 0.05). It also led to an increased release of ACTH and LH in vitro. The results of this study demonstrate the ability of endotoxin to alter pituitary hormone secretion both in vivo and in vitro in sheep, suggesting a direct effect of endotoxin on the pituitary gland.
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PMID:Effect of endotoxin on pituitary hormone secretion in sheep. 826 44


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