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)

Dehydroascorbic acid is present in insignificant amounts in plant and animal tissue but appears in considerable amounts under various physiological and pathological conditions. It is found increased: in blood of patients suffering from infectious diseases; in blood and tissues of thyrotoxic patients; in blood after injection of thyroxin, corticotropin and cortisone. In all the above conditions there is concomitant decrease in L-ascorbic acid and glutathione values of blood and tissues. Dehydroascorbic acid, however, disappears after continued administration of a high dose of ascorbic acid. The accumulation of dehydroascorbic acid seems to be an indication of ascorbic acid deficiency. The extreme sensitivity of the ascorbate system to physiological changes is suggestive of a major biochemical role for this redox system. Accumulated evidences indicate that dehydroascorbic acid possible control cell division.
 ...
PMID:Physiological role of dehydroascorbic acid. 40 55

Reconstitution of 3- to 4-week-old BALB/c nude (nu/nu) mice with 10(7) syngeneic splenocytes, 48 h before intracerebral inoculation with a temperature-sensitive (ts) mutant of VSV (tsG31 KS5), provided protection from the fatal consequences of clinical disease in 80-90% of the infected animals. Reconstitution of animals with 10(7) splenocytes, first depleted of natural killer (NK) cells with anti-asialo GM1 and complement, also afforded protection against the infectious disease. Depletion of T-lymphocytes with anti-thy-1.2 antibody and complement, however, provided little protection with approximately 40% of the animals succumbing to the virus infection within 30 days post-infection. A single intracerebroventricular injection with 14 pM of beta-endorphin, 24 h prior to viral infection, led to an increased fatality of mice previously reconstituted with T-lymphocytes but not in animals receiving only syngeneic NK cells. The increased fatality caused by the neuropeptide was antagonized by naloxone but not beta-endorphin-(1-27). Separation of splenocyte cell populations by buoyant density centrifugation demonstrated that small race lymphocytes, and not the large granular lymphocytes, were responsible for protection of nude mice from the central nervous system infection with ts-VSV. The beta-endorphin-responsive immune cells were shown to be a minor fraction of the small race T-lymphocyte population that bear the asialo-GM1 marker.
 ...
PMID:An immune cell population that responds to beta-endorphin and is responsible for protecting nude mice from the fatal consequences of a virus infection of the central nervous system. 165 24

Infection of lymphocytes with Newcastle disease virus induces the cells to synthesize immunoreactive (ir) adrenocorticotropin (ACTH) and endorphins. The irACTH is synthesized de novo, and common properties of lymphocyte and pituitary ACTH include: antigenicity, bioactivity, molecular weight, and retention time on reverse phase high-pressure liquid chromatography. The irACTH appears to be active in vivo because a rise in serum corticosterone levels in hypophysectomized mice corresponds with spleen cell production of irACTH. Furthermore, preliminary experiments showed that B cell depletion blocked the normal rise in serum corticosterone levels after herpes simplex virus infection of intact mice. It seems that a similar system operates in vivo in humans. Typhoid vaccine, which induces lymphocyte-derived irACTH production in vitro, caused a time-dependent increase in the number of irACTH-positive lymphocytes in both hypopituitarism and normal short children. A rise in serum cortisol levels was seen in one patient with hypopituitarism and all normal patients. The above regulatory circuit also seems able to act in the reverse direction. Pituitary ACTH and alpha-endorphin can behave like lymphokines by being immunosuppressive at 0.5 microM in an in vitro antibody synthesis system. Further, lymphocytes were shown to have high-affinity receptors for both of these hormones. Thus, it appears that the immune and neuroendocrine systems have the ability to signal each other through common or related peptide hormones and receptors.
 ...
PMID:A complete regulatory loop between the immune and neuroendocrine systems. 257 15

Infection of murine splenocytes with Newcastle disease virus results in expression of the proopiomelanocortin gene as determined by dot and northern blot analysis of total cellular and poly(A)+ cytoplasmic RNA. These data provide the first evidence that the precursor protein for adrenocorticotropin and beta-endorphin can be synthesized by lymphoid cells.
 ...
PMID:Newcastle disease virus-infected splenocytes express the proopiomelanocortin gene. 287 61

The adrenal gland functional reserve was studied in a group of 22 patients with active paracoccidioidomycosis before therapy and in 18 of the same patients after termination of six months of ketoconazole treatment. 22 control subjects were also tested. Serum cortisol was measured before and after i.v. infusion of 250 micrograms of corticotropin given over a period of two hours. Basal cortisol levels were subnormal in only one patients before treatment and in four of 18 patients after therapy. Overt Addison's disease was found in 14% of the patients before treatment. However, corticotropin stimulation revealed diminished adrenal reserve in 23% of patients before, and in 44% of the patients after treatment. Although decreased adrenal cortex function after therapy may be influenced by ketoconazole, more studies are needed to determine the role of this agent after prolonged use. The high frequency of subclinical adrenal failure in paracoccidioidomycosis should alert clinicians in charge of such patients, should they face physiological stress.
Infection
PMID:Adrenal function in paracoccidioidomycosis: a prospective study in patients before and after ketoconazole therapy. 300 65

Infection of hypophysectomized mice with Newcastle disease virus caused a time-dependent increase in corticosterone and interferon production. Prior treatment with dexamethasone completely inhibited the virus-induced elevation in corticosterone concentration, but did not significantly alter the interferon response. Lymphocytes appear to be the most likely source of an adrenocorticotropin-like substance that is responsible for the increased corticosterone, since spleen cells from the virus-infected, but not from control or dexamethasone-treated, hypophysectomized mice showed positive immunofluorescence with antibody to adrenocorticotropin-(1-13 amide). Thus the adrenocorticotropin-like material and interferon appear to be coordinately induced the differentially controlled products of different genes. These findings strongly suggest the existence of a lymphoid-adrenal axis.
 ...
PMID:Virus-induced corticosterone in hypophysectomized mice: a possible lymphoid adrenal axis. 618 48

A number of recent studies suggest that interleukin 1 beta (IL-1 beta) is a major mediator of hypothalamo-pituitary-adrenal (HPA) responses following infectious aggression. We investigated whether IL-1 beta mediates long-term changes in HPA activity and studied the cellular regulation of the anterior pituitary. To mimic chronically elevated IL-1 beta production thought to occur during infectious diseases, osmotic pumps (Alzet type) were implanted in the peritoneal cavity of male rats and hIL-1 beta was infused continuously at rates of 1 or 3 micrograms/day. Effects of hIL-1 beta action on plasma ACTH, beta-endorphin (beta-EP) and corticosterone (CORT) secretion and on anterior pituitary (AP), ACTH and beta-EP content were followed. In addition, hypothalamic (HT) CRH mRNA and in AP, CRH receptor (CRH-Rc) mRNA, POMC nuclear primary transcript RNA, POMC nuclear intermediate processing RNA and POMC nuclear and cytoplasmic mRNA were quantified using a highly sensitive solution hybridization nuclease protection assay. Continuous infusion of hIL-1 beta stimulated the HPA axis at varying degrees. Increased HT CRH gene expression, AP POMC gene transcription, ACTH and beta-EP release occurred only during the first 3 days of the treatment. A long-lasting enhancement of ACTH and beta-EP synthesis and of POMC gene expression resulted from activated POMC gene transcription followed by an increased POMC mRNA stability and decreased POMC mRNA turnover. In the AP, stimulation of ACTH and beta-EP secretion and POMC gene transcription disappeared after continuous IL-1 beta treatment, possibly in part due to a refractory process mediated by decreased CRH-Rc gene expression in corticotropes.
 ...
PMID:Effects of continuous infusion of interleukin 1 beta on corticotropin-releasing hormone (CRH), CRH receptors, proopiomelanocortin gene expression and secretion of corticotropin, beta-endorphin and corticosterone. 903 74

Infection with the human immunodeficiency virus (HIV) is associated with a high incidence of cancers. This relationship does not appear to be due to a direct effect of the virus, and may be mediated by neuroimmune interactions since the HIV glycoprotein, gp120, enters the brain soon after infection with HIV, and intracerebroventricular (i.c.v.) infusion of gp120 suppresses aspects of cellular and tumor immunity. It has been speculated that this suppression may be attributed to the release of interleukin-1 (IL-1) in the brain induced by gp120. Using an in vivo tumor model, we examined the effect of centrally administered gp120 on tumor metastasis and lung clearance of mammary adenocarcinoma (MADB106) tumor cells in rats, and the role played by brain IL-1 in mediating these effects. We demonstrate that central administration of gp120 (4 microg) significantly (p<0.05) increased the retention of tumor cells in the lungs and significantly (p<0.02) enhanced the development of tumor metastases. Central administration of IL-1beta (10 ng) also significantly (p<0.05) increased retention of tumor cells in the lungs. The effect of gp120 on lung retention of tumor cells was blocked by co-administration of alpha-melanocyte stimulating hormone (alpha-MSH, 20 ng), a hormone that blocks many of the biological effects of IL-1, or the IL-1 receptor antagonist (50 microg). Given that systemic administration of gp120 or IL-1beta had no effect on the retention of tumor cells in the lungs, these findings indicate that gp120-induced secretion of IL-1 within the brain most likely mediates the effects of gp120 on tumor metastasis. These findings suggest a possible neuroimmune mechanism to account for the increased incidence and aggressiveness of tumors in HIV-infected patients.
 ...
PMID:Intracerebral HIV glycoprotein (gp120) enhances tumor metastasis via centrally released interleukin-1. 950 52

Stress-induced immunological reactions to exercise have stimulated much research into stress immunology and neuroimmunology. It is suggested that exercise can be employed as a model of temporary immunosuppression that occurs after severe physical stress. The exercise-stress model can be easily manipulated experimentally and allows for the study of interactions between the nervous, the endocrine, and the immune systems. This review focuses on mechanisms underlying exercise-induced immune changes such as neuroendocrinological factors including catecholamines, growth hormone, cortisol, beta-endorphin, and sex steroids. The contribution of a metabolic link between skeletal muscles and the lymphoid system is also reviewed. The mechanisms of exercise-associated muscle damage and the initiation of the inflammatory cytokine cascade are discussed. Given that exercise modulates the immune system in healthy individuals, considerations of the clinical ramifications of exercise in the prevention of diseases for which the immune system has a role is of importance. Accordingly, drawing on the experimental, clinical, and epidemiological literature, we address the interactions between exercise and infectious diseases as well as exercise and neoplasia within the context of both aging and nutrition.
 ...
PMID:Exercise and the immune system: regulation, integration, and adaptation. 1089 31

The biology of leptin has been studied most extensively in rodents and in humans. Leptin is involved in the regulation of food intake, energy homeostasis and immunity. Leptin is primarily produced in white adipose tissue and acts via a family of membrane bound receptors, including an isoform with a long intracellular domain (OB-Rb), and many isoforms with short intracellular domains (Ob-Rs). OB-Rb is predominantly expressed in the hypothalamic regions involved in the regulation of food intake and energy homeostasis. The other isoforms are distributed ubiquitously and are found in most peripheral tissues in far greater abundance than OB-Rb. The effects of leptin on food intake and energy homeostasis are central and are mediated via a network of orexigenic neuropeptides (neuropeptide Y, galanin, galanin-like peptide, melanin-concentrating hormone, orexins, agouti-related peptide) and anorexigenic neuropeptides (corticotropin-releasing hormone, pro-opiomelanocortin, alpha-melanocyte stimulating hormone and cocaine- and amphetamine-regulated transcript). In addition, leptin acts directly on immune cells to stimulate hematopoesis, T-cell immunity, phagocytosis, cytokine production, and to attenuate susceptibility to infectious insults. Emerging data in ruminants suggest that leptin is dynamically regulated by many factors and physiological states. Thus, leptin is secreted in a pulsatile fashion, but without a marked diurnal rhythm. A positive relationship between adiposity and plasma leptin concentration exists in growing and lactating ruminants. The concentration of plasma leptin increases during pregnancy, starts to decline 1--2 wk before parturition, and reaches a nadir in early lactation. The reduction of plasma leptin at parturition is likely to promote centrally mediated adaptations required in periods of energy deficit, but could have negative effects on immune cell function. Future research is needed in ruminants to address the roles played by leptin and the central nervous system in orchestrating metabolism during the periparturient period and during infectious diseases.
 ...
PMID:Leptin and the regulation of food intake, energy homeostasis and immunity with special focus on periparturient ruminants. 1187 19


1 2 Next >>