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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The material presented here summarizes the bulk of the presently available immunologic data bearing upon the in vivo relationship between brown adipose tissue and the immune system. The experiments were carried out in rats adipectomized (by surgical excision of the interscapular brown adipose tissue at birth), thymectomized (by neonatal removal of the thymus), adipectomized and thymectomized, and corresponding sham-operated controls. The following immune phenomena were studied: antibody production to soluble and corpuscular antigens; Arthus and delayed hypersensitivity skin reactions to bovine serum albumin; rejection of allogeneic skin and thyroid grafts; lymph node enlargement in a host-versus-graft reaction; experimental allergic encephalomyelitis and thyroiditis; immune response in normal animals treated with extracts from brown adipose tissue; allergic encephalomyelitis in thymoadipectomized animals; plaque-forming cell response and hemagglutinating antibody titers in animals injected with met-enkephalin and leu-enkephalin; and survival rate of adipectomized mice inoculated with Sarcoma-I cells. The results indicated that the cell-mediated immune reactions were potentiated in adipectomized rats. Antibody production was not significantly changed by neonatal adipectomy. Adipectomized mice, inoculated with Sa-I tumor cells, survived longer than controls, thus indicating that adipectomy made possible the recognition of discrete histocompatible differences between Sa-I cells and A/JAX mice. Adipectomy increased the ability of rats to develop autoimmune diseases. Saline extracts from brown adipose tissue of newborn rats suppressed hypersensitivity skin reactions in normal adult rats. Thymoadipectomized rats showed an almost normal ability to develop allergic encephalomyelitis, a finding that suggested that the potentiating influence of adipectomy on encephalomyelitis was neutralized by thymectomy. It appears that brown adipose tissue functions as a natural antagonist of the thymus. Enkephalins were found to be more effective immunosuppressors in adipectomized than in normal animals. The last finding establishes a functional link between brown adipose tissue and neuropeptides. It seems that the potentiation of immune response in adipectomized animals is effected by altered release of yet unidentified mediators and modulators. The evidence indicates that brown adipose tissue, in which neurohumoral activity occurs, may be an important component of an integrated immunoneuroendocrine system.
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PMID:Brown adipose tissue. Its in vivo immunology and involvement in neuroimmunomodulation. 330 Apr 71

The in vitro priming of mouse spleen cultures with sheep erythrocytes (SE) was used to study the modulation of immune function by met-enkephalin (MENK). In these studies, suboptimal, optimal, and supraoptimal concentrations of SE were used to manipulate the plaque-forming cell (PFC) responses of cultured spleen cells. MENK, at a concentration of 10(-7) M, was able to abolish the high antigen dose-induced suppression of the PFC response, but was unable to increase the PFC response of cultures treated with suboptimal doses of antigen. On rare occasions when the supraoptimal dose of antigen did not suppress the immune response, the addition of 10(-7) M MENK to the culture medium suppressed the PFC response. Naloxone was unable to block the effect of MENK. These results indicate that the nature of the immune response must be taken into consideration when evaluating the effect of opioid peptides on immune function. We propose that MENK possesses a dual modulatory role, with the abilities to suppress a strong immune response and reverse high antigen-induced immunosuppression.
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PMID:Modulation of the in vitro murine immune response by met-enkephalin. 345 8

B-cell differentiation was studied in patients with MS and in age- and sex-matched controls, using a pokeweed mitogen (PWM)-stimulated in vitro culture system. Peripheral blood lymphocytes were obtained and separated into T-cell and non-T-cell fractions. Autologous and allogeneic combinations of T cells and B cells were cultured in the presence of pokeweed mitogen for 7 days. Numbers of plaque-forming cells (PFC) were measured at the end of the culture period. T cells from MS patients before and after a 10-day course of adrenocorticotropic hormone (ACTH) were able to cooperate fully in the generation of PWM-generated PFC. B cells from MS patients showed a decreased ability to differentiate into PFC in the presence of either autologous or allogeneic T cells. No significant change in differentiation was observed after a 10-day course of intravenous ACTH. We were thus unable to demonstrate any alteration in T-cell function in MS but were able to demonstrate a decreased ability of MS B cells to differentiate into immunoglobulin-secreting cells. ACTH had no significant effect on these abnormalities.
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PMID:B-cell differentiation in multiple sclerosis and the effect of intravenous ACTH. 630 Jul 31

The effects of opioid peptides on immune responses were investigated. It was found that beta-endorphin (beta-END) can depress proliferative responses to PHA in rat splenocytes but enhance those in mice, and it could also inhibit the plaque-forming cell (PFC) response to sheep red blood cells when mouse splenocytes immunized in vivo were cultured in vitro with the peptide. The peptide antagonist naloxone was able to reverse beta-END suppression of the PFC response. The data indicate that beta-END suppresses antibody production or secretion via a specific opioid-receptor-mediated mechanism.
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PMID:Effects of beta-endorphin on phytohemagglutinin-induced lymphocyte proliferation and mouse plaque-forming cell response via an opioid receptor mechanism. 771 65

Central catecholamine alterations associated with immune activity are similar to those seen following stressor exposure. Inasmuch as aged animals exhibit more pronounced stressor-provoked alterations of central amines relative to younger animals, it was of interest to determine whether immune challenge would similarly induce more pronounced central amine variations in older animals. Fifteen-month old CD-1 mice challenged with 10(7) sheep red blood cells (SRBC) revealed an equivalent peak splenic plaque-forming cell response (4 days after antigen challenge) to that of 3-month-old mice challenged with 10(6) cells. Neither plasma adrenocorticotropic hormone (ACTH) nor corticosterone levels varied over days following immunization, although ACTH levels were generally higher in the older mice. In both age groups reductions of hypothalamic and locus coeruleus norepinephrine (NE) and increased accumulation of the metabolite MHPG coincided with (or preceded by 24 h) the peak immune response. However, increased accumulation of MHPG in the hypothalamus was greater and occurred earlier in the locus coeruleus of the aged mice. Likewise, at or about the time of peak immune responses nucleus accumbens dopamine (DA) levels were reduced and metabolites elevated in both age groups, while in the prefrontal cortex only DA metabolite levels were elevated. These data are commensurate with previous findings showing that SRBC inoculation may influence central neurotransmitters and that such effects correspond with the time of the peak immune responses. Moreover, in so far as hypothalamic NE utilization is concerned, it seems that the effects of SRBC inoculation are more pronounced in aged animals.
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PMID:Alterations in central catecholamines associated with immune responding in adult and aged mice. 788 70

Serum beta-endorphin was quantified by radioimmunoassay in 71 patients with psoriasis vulgaris, other chronic inflammatory skin diseases with T-cell infiltrates [atopic dermatitis (n = 25), and systemic sclerosis (n = 34)], and 100 healthy subjects. The neuropeptide was found to be markedly (P < 0.001) increased in patients with psoriasis (14.4 pg/ml), atopic dermatitis (9.2 pg/ml) and systemic sclerosis (9.8 pg/ml) compared with normal controls (6.1 pg/ml). The highest values of beta-endorphin were found in patients with actively spreading plaque psoriasis (17.3 pg/ml), whereas lesion-free patients showed a reduction in neuropeptide concentration (10.2 pg/ml). The levels were much higher in patients with widespread psoriatic lesions (> 60% body surface; 16.2 pg/ml), which lasted longer than 3 months (15.8 pg/ml), whereas neither the presence of stress nor itching correlated with the serum peptide concentration. Our data suggest that beta-endorphin is produced in psoriatic lesions by inflammatory cells, rather than the increased levels being the result of activation of the pituitary-adrenal axis by chronic stress. The generation of neuropeptide in psoriatic lesions and its antinociceptive effect on the peripheral sensory nerves might explain why pruritus is a relatively rare phenomenon in psoriasis.
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PMID:Increased concentration of beta-endorphin in sera of patients with psoriasis and other inflammatory dermatoses. 791 92

Proopiomelanocortin (POMC)-producing cells comprise nearly 100% of the adult rat intermediate lobe (IL) hormone-producing cells. Secretion by these cells in the adult is primarily under negative regulation by dopamine. Although the POMC-derived peptide alpha-MSH has been detected in plasma of fetal rats, the secretory capability of fetal melanotrophs has not yet been examined directly. Here we have used the reverse hemolytic plaque assay to assess, at the single-cell level, basal and regulated release by melanotrophs from fetal and early postnatal ages. Basal secretion was detected at the earliest age examined [Embryonic Day 17.5 (e17.5)], but CRH (10(-8) M) stimulated secretion was not observed until e19.5. As development proceeded, CRH increased both individual plaque sizes and the percentage of melanotrophs stimulated to secrete. An unexpected, transient inhibition of CRH stimulated release from melanotrophs by dexamethasone (DEX, 10(-6) M) was observed from e19.5-p2 (postnatal Day 2). By p3, however, DEX no longer inhibited melanotroph secretion while inhibition of CRH-stimulated release from p3 corticotrophs was readily detected. The dopamine agonist ergocryptine (ERG, 10(-6) M) inhibited basal secretion from melanotrophs, but not corticotrophs, at all ages examined. Taken together, these results indicate that melanotrophs undergo a maturation process in which they are initially nonresponsive to CRH, next possess functional CRH and steroid receptors, and finally, undergo functional uncoupling of steroid receptors which characterizes the adult IL. The loss of steroid-mediated inhibition of stimulated secretion parallels the arrival of catecholaminergic input into the IL. In contrast, the early response of melanotrophs to dopaminergic agonists, which can be detected 1 week prior to arrival of catecholaminergic fibers into the neurointermediate lobe, appears to be an intrinsic feature of these cells that is never present in corticotrophs.
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PMID:Ontogeny of basal and regulated proopiomelanocortin-derived peptide secretion from fetal and neonatal pituitary intermediate lobe cells: melanotrophs exhibit transient glucocorticoid responses during development. 857 13

Proopiomelanocortin (POMC)-producing cells are present in both the anterior (AL) and intermediate (IL) lobes of the adult rat pituitary. Both cell types are derived from a single embryonic rudiment, Rathke's pouch, and synthesize the same hormone precursor, POMC, but differ in the pattern of precursor processing and regulation of peptide secretion. Here we have used the reverse hemolytic plaque assay to determine the ontogeny of basal and regulated secretion by AL POMC cells. Basal secretion of beta-endorphin was first observed at Embryonic Day 13.5 (e13.5), the age when POMC-derived peptides were first detected immunocytochemically. Peptide secretion stimulated by corticotropin releasing hormone (CRH; 10(-8) M) was first detected at e15.5. The CRH-stimulated secretion involved two different components: (1) an increase in the amount of hormone secreted per cell (increase in plaque size) as well as (2) an increase in the number of plaque-producing cells. The greatest stimulation by CRH was observed at e16.5, a time when AL POMC mRNA levels increase significantly and when CRH neurons are first detected immunocytochemically in the hypothalamus. CRH-stimulated secretion, but not basal release, was inhibited by preincubation with dexamethasone (DEX; 10(-6) M) as early as e15.5, while the dopamine agonist ergocryptine (ERG; 10(-6) M) did not alter basal or CRH-stimulated release at any age studied. These results demonstrate that AL POMC cells are capable of hormone secretion as early as POMC peptides are first detected immunocytochemically and that these cells respond in an adult-like manner to physiological regulators soon after their initial appearance. Moreover, these responses remain unaltered during the early postnatal stress-nonresponsive period, suggesting that deficits at this time must lie at a level other than the corticotroph. Taken together, these results show that AL POMC cells possess functional regulatory receptor systems prior to maturation of the hypothalamic-hypophyseal portal system.
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PMID:Ontogeny of basal and regulated secretion from POMC cells of the developing anterior lobe of the rat pituitary gland. 857 41

Reported studies using the conventional pituitary cell culture technique suggest that beta-endorphin (B-EP) produced locally in the pituitary or reaching it from the hypothalamus acts in conjunction with estradiol (E2) to initiate and in conjunction with progesterone (P4) to terminate the midcycle surge of LH. In addition, the reverse hemolytic plaque assay (RHPA) was used to investigate the effects of E2 and P4 on the secretory activity of individual pituitary cells. The results of these experiments indicate that 1) E2 enhances the secretion of LH, ACTH, and B-EP by individual pituitary cells; 2) E2 increases the number of secreting cells for each of the three hormones; 3) the rise in B-EP and ACTH secretion antecede that of LH; 4) P4 augments ACTH and B-EP secretion by individual pituitary cells; and 5) P4 has dual effects, acutely (1 h) potentiating LH secretion from already active cells and subsequently (8 h) recruiting cells that formerly had little or no secretory activities. Collectively, the above studies support a role for steroid hormones in regulation of midcycle LH secretion at the pituitary level. The results also suggest that intrapituitary (paracrine/autocrine) and extrapituitary (endocrine) B-EP modulates gonadal steroid effects on LH secretion by pituitary gonadotrophs.
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PMID:The interaction between beta-endorphin and gonadal steroids in regulation of luteinizing hormone (LH) secretion and sex steroid regulation of LH and proopiomelanocortin peptide secretion by individual pituitary cells. 900 99

We describe the construction and screening of a random peptide library displayed by filamentous phage. The peptides are expressed in multiple copies on the filamentous phage M13 as amino-terminal fusions with the major coat protein, the product of gene VIII. These libraries are efficiently screened for reactive peptides, using a combination of panning in solution followed by a plaque lift assay. Advantages of this system are that both high- and low-affinity phage clones are simultaneously identified and the analysis of non-reactive phage is minimized. The vector system utilized to construct this library enables it to be used for the construction of peptide libraries employing a combinatorial cloning strategy. This feature makes it especially suitable for construction of peptide libraries using codon-based oligonucleotide synthesis. The vectors also allow rapid optimization and modification of lead peptides by codon-based mutagenesis. A 20-amino acid long random peptide library of 1 x 10(9) members was constructed and screened for peptides that bound to (i) a monoclonal antibody recognizing the amino-terminus of beta-endorphin; (ii) a monoclonal antibody recognizing a peptide epitope derived from the v-ros oncogene product; and (iii) the constant region of murine IgG2b. The approach described here provides a means for the construction of customized libraries that can be screened with a variety of target molecules.
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PMID:A combinatorial method for constructing libraries of long peptides displayed by filamentous phage. 923 93


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