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)

Evidence for interactions between the nervous and immune systems arises from a number of experimental observations: the behavioral conditioning of immune responses, the effects of stimulation or lesion of brain sites on immune system function, the effects of stressors on immune responses and tumor growth, and physiological and neurochemical changes in the brain during immune responses. The links between the nervous and immune systems probably include glucocorticoids secreted from the adrenal gland, catecholamines and neuropeptides secreted by sympathetic terminals and the adrenal medulla, certain pituitary and gonadal hormones, and polypeptides produced by cells of the immune system. The effect of glucocorticoids is not exclusively immunosuppressive, nor is it adequate to explain all the effects of stress. The effects of opiates on immune function are complex; in vitro, endogenous opiates most often facilitate immune activity, but in vivo, opiates appear to inhibit immune responses and impair tumor rejection. The in vitro effects are rarely prevented by naloxone pretreatment and appear to require the integrity of the C- rather than the N-terminal of beta-endorphin, suggesting a nonopiate character. Infections or the administration of antigens increase circulating concentrations of glucocorticoids and activate cerebral catecholaminergic metabolism, especially in the hypothalamus. These responses suggest that challenges to the immune system are physiologic stressors. Interleukin-1 (IL-1) produced by immune cells may be the mediator of these effects, thus acting as an "immunoneurotransmitter". The cerebral responses suggest that the brain can monitor the progress of immune responses. IL-1 and the glucocorticoids together may form a regulatory feedback mechanism for immune responses.
 ...
PMID:Psychoneuroimmunology for the psychoneuroendocrinologist: a review of animal studies of nervous system-immune system interactions. 268 23

Infections are associated with increased plasma concentrations of adrenocorticotropic hormone (ACTH) and corticosterone. Hypothalamo-pituitary-adrenal (HPA) responses have also been observed with immunological stimuli that are not infective. Although such responses have been suggested to be mediated by ACTH secreted by lymphocytes, adrenocortical activation by immunological stimuli requires a functional pituitary. The most likely mechanism by which immunological stimuli activate the HPA axis involves production of cytokines by lymphocytes. The prime candidate is interleukin 1 (IL-1), because IL-1 production follows activation of the immune system and IL-1 administration is a potent activator of the HPA axis. However, other cytokines, such as tumour necrosis factor, may also be involved. Most immunological stimuli and IL-1 also activate both peripheral and central noradrenergic neurons. IL-1-induced activation of the HPA axis in vivo depends upon secretion of corticotropin-releasing factor (CRF), an intact pituitary, and the ventral noradrenergic bundle which innervates the CRF-containing neurons in the paraventricular nucleus (PVN) of the hypothalamus. Besides elevating body temperature, administration of IL-1 elicits a number of behavioural responses in rats and mice, including anorexia, increased sleep time, decreased investigation of novel objects and other animals, increased defensive withdrawal and other behaviours characteristic of sickness. Some of these responses can be reversed by CRF-antagonists and mimicked by CRF administration. Thus, endogenous production of IL-1 can account for a range of physiological and behavioural responses characteristic of sickness. Nevertheless, definitive evidence that IL-1 mediates these responses in sick animals is lacking.
 ...
PMID:Infection as a stressor: a cytokine-mediated activation of the hypothalamo-pituitary-adrenal axis? 849 Oct 88

The purpose of this article is to provide information about the exercise-induced alterations of cellular immune parameters depending on the intensity related to the individual anaerobic threshold (IAT) and duration of exercise. Immunological parameters were differential blood counts (CD14, CD45), monocyte subpopulations (CD14, CD16), lymphocyte subpopulations (CD3, CD4, CD8, CD45RO, CD19, CD16, CD56, HLA-DR) and natural killer cells (CD3, CD16, CD56), oxidative burst activity of neutrophils, and phagocytosis of neutrophils (flow cytometry). The main results were: (a) "Moderate" exercise (duration < 2h at about 85% of the IAT corresponding to a lactate steady state at about 2 mmol.l-1, < 30 min at the IAT corresponding to a lactate steady state of 4 mmol.l-1) elicits lower changes in cell concentrations and hormonal responses than strenuous exercise [exhaustive exercise at 100% IAT or above; (exhaustive) long-term (> 2-3h) endurance exercise]. Similar investigations about cell functions to decide about the positive or negative nature of these observations will have to follow in the future. (b) The neutrocytosis following exercise is more dependent on the duration than on the intensity of exercise. Especially exercise sessions that lead to a strong incline of the adrenocorticotropic hormone, beta-endorphin and cortisol are associated with this neutrocytosis. (c) Neutrophils' function during the exercise-induced neutrocytosis indicated by phagocytosis and oxidative burst activity is unchanged or reduced following strenuous endurance exercise, whereas bacterial URTI leads to similar neutrophil counts but significantly increased cell activities indicating the diverse meaning of the leukocytosis in infections (primed cells, enhanced cell activity, stimulated defense mechanism) and following exercise (impaired cell function, suppressed defense mechanism). (d) Regular monocytes (early differentiation stage) are strongly recruited into the circulation during long-term aerobic exercise, whereas mature monocyte cell counts (premacrophages) increase most with highly intensive (an)aerobic exercise above the IAT. Infections induced a maturation from regular to mature monocytes as a response to the infectious antigenic stimulus, whereas exercise does not, indicating the diversity between change of cell counts and function. (e) Long-term endurance diverse meaning leads to increases of activated CD45RO+ T cells (memory cell phenotype) but compared to the incline of cell concentrations and activation levels (% HLA-DR+ T cells) during infections like infectious mononucleosis this effect is small indicating only minor effects on T cell function by exercise. The effect of single bouts of exercise on immune cell counts is large but the effects on the cell function is - i.e. compared to bacterial URTI - relatively small.
 ...
PMID:The acute immune response to exercise: what does it mean? 912 61

Practical relevance: Hyperadrenocorticism (HAC) is a relatively uncommon endocrinopathy of older cats, with a mean age at diagnosis of 10 years. In addition to pituitary-dependent and adrenal-dependent hypercortisolism, clinical signs of HAC can result from adrenal sex steroid-producing tumours. Clinical challenges: While HAC in cats has many similarities to canine HAC, there are key differences in presentation, diagnosis and response to therapy. Most, but not all, cats with HAC have concurrent diabetes mellitus, which is often insulin resistant. Up to a third of cats with HAC have extreme skin fragility and are at high risk of debilitating iatrogenic skin tears during diagnostic or therapeutic interventions. Infections of the skin and nail beds, and urinary, respiratory and gastrointestinal tract, secondary to cortisol-induced immune suppression, are also common. Cats respond differently to dogs to adrenal function tests including adrenocorticotropic hormone (ACTH) stimulation and dexamethasone suppression tests; a 10-fold higher dose of dexamethasone is recommended in cats to screen for HAC. Curative treatment options include adrenalectomy or transsphenoidal hypophysectomy. Radiation or medical treatment may improve clinical signs. The response to mitotane therapy is poor. While trilostane is the medical treatment of choice based on retrospective studies, investigations into the pharmacokinetics of this drug in cats are lacking. Global importance: Feline HAC occurs worldwide and is not associated with any purebreed predisposition. Although uncommon, adrenal sex steroid-producing tumours have a higher prevalence in cats than in dogs. Evidence base: The information in this review is drawn from over 180 reported cases of feline HAC. Reports investigating clinical presentation, clinicopathological findings and treatment outcomes are observational, retrospective multiple case series (EBM grade III) or single case reports (EBM grade IV). While most endocrine testing studies for diagnosis are cohort controlled analytical studies (EBM grade III), prospective, randomised, placebo-controlled studies have been performed (EBM grade I).
 ...
PMID:Peculiarities of feline hyperadrenocorticism: Update on diagnosis and treatment. 2991 79