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)

This in vitro study examined the effects of interleukin-1 (IL-1) and interferon-gamma (Ifn-gamma) on the release of cholecysto-kinin (CCK) from superfused hypothalamo-neurohypophyseal complexes (HNC) of rats. An increase of CCK from HNC was elicited in a dose-dependent manner by recombinant human IL-1 alpha and -1 beta in concentrations of 0.1-10 nM. In contrast, the release of CCK from HNC was not affected by recombinant human Ifn-gamma at any dose tested (0.1, 1 and 10 nM). The increased release of CCK elicited by IL-1 was calcium-dependent, as was that induced by potassium (60 mM), but it was biphasic and had a different time course and a lower magnitude than those induced by potassium and veratridine. These results suggest that IL-1 activates pituitary-adrenal axis by stimulating CCK neurons in the hypothalamus and/or neurohypophysis to release CCK, since CCK has been implicated in the regulation of adrenocorticotropin release.
 ...
PMID:Stimulation of cholecystokinin (CCK) release from superfused rat hypothalamo-neurohypophyseal complexes by interleukin-1 (IL-1). 145 18

To investigate phagocytosis, an assay enabling flow cytometric analysis of single cells having internalized fluorescent carboxyl microspheres was employed. Greater than 80% of murine testicular Sertoli line (TM4) cells were found to phagocytose one or more microspheres within six hours and electron microscopy confirmed carboxyl microsphere internalization. This level was equivalent to that of a macrophage-like cell line and much greater than the levels of testicular Leydig (TM3) cells. Reducing extracellular calcium or using a calcium channel blocker profoundly inhibited phagocytosis suggesting that phagocytosis by Sertoli cells requires extracellular Ca++. Although follicular stimulating hormone, luteinizing hormone, and testosterone had no significant effects on Sertoli cell phagocytosis, insulin, epidermal growth factor, and hydrocortisone enhanced activity. In contrast, beta-endorphin and 8-bromoadenosine-cyclic monophosphate had an inhibitory effect. In contrast to augmenting macrophage phagocytosis, 1,25-(OH)2D3, interferon-gamma, prostaglandin E2, and lipopolysaccharides, had no apparent effect on that by Sertoli cells. Additionally, neither C3bi receptors (Mac-1 antigen) nor FcRII could be detected on Sertoli cells. In total, the findings demonstrated that the murine Sertoli line exhibits potent phagocytic function and suggest the regulation of this activity may differ from that in "professional" phagocytic cells.
 ...
PMID:Phagocytosis by the murine testicular TM4 Sertoli cell line in culture. 153 Aug 70

Interactions between opiates and the human immune system have important clinical implications. To further evaluate these interactions, we studied in vitro and in vivo effects of morphine sulfate (morphine) and beta-endorphin (Bend) on antibody-dependent cell cytotoxicity (ADCC), natural killer cell cytotoxicity (NKCC), and effector cell expression of antibody Fc receptors. Morphine and Bend had no potent in vivo or in vitro effect on FcR expression nor did they have a significant in vitro effect on ADCC by monocytes or polymorphonuclear cells. Bend enhancement of NKCC in vitro was inhibited by coincubation of effector cells with morphine. After taking 90 to 150 mg of oral morphine, study volunteers demonstrated a significant decrease in ADCC by peripheral blood mononuclear cells. The same individuals demonstrated a consistent increase in NKCC and no change in the expression of Fc receptors. Effector cells from these individuals responded normally to in vitro incubation with interferon-gamma (IFN-gamma).
 ...
PMID:Effect of morphine and beta-endorphin on human Fc receptor-dependent and natural killer cell functions. 154 Oct 57

Recent evidence has suggested that stress may suppress the immune system and increase the frequency and severity of viral and neoplastic disease. The mechanisms for stress-induced modulation of immune function are unclear, but several neuropeptides are thought to be involved. Because macrophages play an important role in the host defense against infection and neoplasia, several stress-related neuropeptides were screened in efforts to determine whether these substances affect macrophage-mediated tumoricidal activity. Adrenocorticotropin and noradrenaline each completely blocked the capacity of mouse recombinant interferon-gamma (INF-gamma) to activate murine peritoneal macrophages to a tumoricidal state as measured by the lysis of 125I-UdR-labeled melanoma target cells. Vasoactive intestinal peptide significantly potentiated the suppressive effects of noradrenaline. In contrast, neurotensin markedly enhanced the cytolytic capability of peritoneal macrophages activated with INF-gamma. Several other neuropeptides, including substance P, alpha-endorphin, beta-endorphin, Leu-enkephalin, and Met-enkephalin, had no effect on macrophage activation. These findings demonstrate that selected stress-related neuropeptides and neurohormones significantly modulate the capacity of macrophages to attain a tumoricidal state and suggest that alteration of macrophage function by neuropeptides may be a prominent feature of stress-induced enhancement of neoplastic disease.
 ...
PMID:Modulation of macrophage-mediated tumoricidal activity by neuropeptides and neurohormones. 258 37

The stress-responsive neuropeptide beta-endorphin (beta-END) has been shown to either enhance or suppress interferon-gamma (IFN-gamma) production by mitogen stimulated peripheral blood mononuclear cells (PBMNC) in vitro. In this study, we investigated whether donor selection and the medium used for cell culture influenced the modulatory effect of beta-END on the IFN-gamma production by PBMNC. Considerable variation of the effect of beta-END on IFN-gamma production was observed in individuals who underwent multiple testing. Suppression of IFN-gamma was significantly greater in 16 male donors (29 +/- 6.0%) compared to 8 female donors (1.5 +/- 6.4%) when PBMNC were preincubated for 3 h with beta-END followed by concanavalin A stimulation for 72 h in medium containing 20% fetal bovine serum (FBS). Lowering the concentration of FBS resulted in enhanced production of IFN-gamma by PBMNC exposed to beta-END. Arachidonic acid or beta-END added separately to medium containing 3% autologous serum produced no suppression of IFN-gamma, but when added together resulted in significant suppression. This observation provides support for the hypothesis that beta-END achieves its suppressive effect on IFN-gamma via a mechanism involving arachidonic acid metabolism. We conclude that the modulatory effect of beta-END on IFN-gamma production by PBMNC is both donor and medium dependent.
 ...
PMID:Modulatory effects of beta-endorphin on interferon-gamma production by cultured peripheral blood mononuclear cells: heterogeneity among donors and the influence of culture medium. 297 92

Herpes simplex viruses (HSV) remain latent in sensory and peripheral ganglia and can be reactivated to cause recurrent HSV infections. Recent evidence has suggested that stress can induce an immunosuppressive state and increase the frequency and severity of recurrent herpes infections. Because macrophages play a central role in the host defense against HSV, the effects of stress-related neuroendocrine hormones on macrophage-HSV interactions were examined. Norepinephrine and epinephrine blocked the capacity of recombinant interferon-gamma (IFN-gamma) to activate murine macrophages to a cytotoxic state capable of selectively killing HSV-infected cells. In contrast, ACTH, dopamine, serotonin, and beta-endorphin had no effect. The suppression of IFN-gamma-induced, macrophage-mediated lysis of HSV-infected cells occurred concomitantly with a marked increase in macrophage intracellular cyclic AMP levels. Moreover, exogenous administration of dibutyryl cyclic AMP blocked induction of macrophage-mediated cytotoxicity, suggesting that the neurohormones were modulating macrophage function via an adrenergic receptor-mediated system. These findings demonstrate that selective stress-related neurohormones modify the cytolytic activity of macrophages against virus-infected cells and suggest a possible neuroendocrine-immunologic basis for the recurrence of HSV infection.
 ...
PMID:Neuroendocrine hormones suppress macrophage-mediated lysis of herpes simplex virus-infected cells. 300 Nov 83

Mounting evidence suggests that opiate addiction and stress are associated with impaired cell-mediated immunity. We tested the hypothesis that morphine and the endogenous opioid beta-endorphin (beta-END), a pituitary peptide released in increased concentrations during stress, can suppress the production of the key macrophage-activating lymphokine interferon-gamma (IFN-gamma) by cultured human peripheral blood mononuclear cells (PBMNC). Using a radioimmunoassay to measure IFN-gamma, we found that exposure of PBMNC to biologically relevant concentrations of both opioids significantly inhibited IFN-gamma generation by cells stimulated with concanavalin A and varicella zoster virus. Studies of the mechanism of suppression revealed (a) a classical opioid receptor is involved (suppression was antagonized by naloxone and was specific for the NH2 terminus of beta-END), (b) monocytes are the primary target cell for opioids (monocyte-depleted lymphocyte preparations showed little suppression), and (c) reactive oxygen intermediates (ROI) and prostaglandin E2 are important mediators (scavengers of ROI and indomethacin eliminated the suppression). Based on these findings we suggest that opioid-triggered release of inhibitory monocyte metabolites may play a role in the immunodeficiency associated with narcotic addiction and stress.
 ...
PMID:Opioid-mediated suppression of interferon-gamma production by cultured peripheral blood mononuclear cells. 304 Aug 7

Studies on neuroendocrine hormone receptor have been hampered by low numbers and concentrations of receptors found within and outside the neuroendocrine system. The complementary peptide approach is particularly useful for dealing with this problem and has been used to characterize lymphoid receptors for arginine vasopressin (AVP), corticotropin (ACTH), substance P, and opioid peptides. A nonapeptide derived by reading of the complementary DNA strand of the bovine AVP gene in the 3' to 5' direction specifically blocks the AVP helper signal for interferon-gamma production by mouse T lymphocytes. Antibodies to 3'-5' AVP-binding peptide bound to cells, and the binding was inhibited by excess AVP. Thus, binding of anti-3'-5'AVP-binding peptide antibodies to the AVP receptor was specific. The complementary peptide approach has also been used to produce antibodies specific for the ACTH receptor complex. Complementary peptides to ACTH derived by reading in either the 5' to 3' or 3' to 5' direction were able to bind to ACTH. Monospecific antibodies to the ACTH (1-24) complementary peptide caused an ACTH-like steroidogenic response of cultured mouse adrenal cells, presumably by binding to the ACTH receptor, and binding was specifically inhibited by ACTH. The ACTH receptor complex from solubilized adrenal cells was shown to consist of four subunits with M(r) 83,000, 64,000, 52,000, and 22,000. The 83,000 and 52,000 M(r) subunits are disulfide linked and noncovalently associated with the other subunits, with binding of labeled ACTH localized to the 83,000 M(r) subunit. Similarly, a complementary peptide was shown to bind directly to substance P in a saturable and dose-dependent manner.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Complementary peptides as probes to explore neuropeptide receptors on lymphocytes. 787 40

We recently demonstrated that the opioid peptide beta-endorphin (beta-End) has the capacity to stimulate interleukin-2 (IL-2) and IL-4 production by murine CD4+ T cells. Since opioid peptides have been demonstrated to contain stimulatory as well as inhibitory sites, we studied peptide fragments of beta-End to identify a moiety with exclusive stimulatory capacity. To this end, the effects of various opioid peptides on the production of IL-2, IL-4, IL-6, and interferon-gamma (IFN-gamma) by CD4+ T cells were determined. It appeared that two peptide fragments of beta-End, i.e., beta-End6-31 and beta-End18-31, that lack the N-terminal enkephalin part, enhanced IL-2 and IL-4 production to a similar extent as intact beta-End, indicating that the N-terminal part is not involved in the stimulating effects of beta-End. Also the production of IL-6 and IFN-gamma was increased by these peptides. By contrast, the fragments beta-End24-31 and beta-End28-31 did not stimulate the production of the cytokines. Surprisingly, also alpha-End, which is equivalent to beta-End1-16 and hence lacks the sequence comprising amino acids 18 through 31, was stimulatory. This effect was not prevented by naloxone, indicating that opioid receptors were not involved. Moreover, methionine-enkephalin (Met-Enk), which binds to opioid receptors, did not affect cytokine production. Because both alpha-End and beta-End18-31 stimulate cytokine production by CD4+ T cells and do not overlap is sequence, it is concluded that at least two distinct sites of beta-End can exert stimulating effects on cytokine production.
 ...
PMID:Identification of distinct sites of beta-endorphin that stimulate lymphokine production by murine CD4+ T cells. 791 52

1. Interleukin-10 (IL-10) has a wide range of activities in the immune system such as modulation of interferon-gamma (IFN-gamma) and antibody production. The neuropeptide hormone corticotropin (ACTH) has similar activities, suggesting that a bidirectional communication mechanism operates between the immune and the neuroendocrine system involving these two substances. 2. Murine pituitary tumor cells (AtT-20) were found to produce up to 3 ng/ml of IL-10. 3. Pituitary cell corticotropin production was enhanced by IL-10 treatment. 4. IL-10 induced the production of ACTH in mouse splenocytes. 5. Authenticity of pituitary-derived IL-10 was shown by the demonstration of identical nucleic acid sequences of reverse-transcribed, polymerase chain reaction amplified fragments of cDNA obtained from murine splenocytes, a murine pituitary tumor cell line, and freshly isolated murine pituitaries.
 ...
PMID:Evidence for the production and action of interleukin-10 in pituitary cells. 795 60


1 2 3 4 5 Next >>