Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several lines of evidence suggest that the anterior pituitary hormone prolactin has a stimulatory role on immune function and that pharmacological suppression of prolactin secretion with the dopamine-agonist bromocriptine suppresses both humoral and cellular immunity. Here, we describe the effects of prolactin-suppression on the course of experimental allergic encephalomyelitis in female Lewis rats. Initiation of continuous bromocriptine treatment before immunization reduced both the severity and incidence of clinical signs of acute experimental allergic encephalomyelitis. Experimental allergic encephalomyelitis-immunized rats experienced a threefold rise in basal prolactin levels on day 4 after immunization and maintained elevated prolactin levels on day 10, before the onset of neurological signs of experimental allergic encephalomyelitis. Bromocriptine treatment reduced prolactin levels to those of sham-immunized rats. In vivo bromocriptine pretreatment inhibited splenic lymphocyte proliferative responses in vitro to the immunizing antigen and to concanavalin A. Moreover, bromocriptine therapy was protective when initiated 1 week after the initial immunization and was also effective in suppression of late disease. These results indicate that (1) prolactin levels are elevated after immunization and before the onset of experimental allergic encephalomyelitis, (2) bromocriptine inhibits both prolactin secretion and the severity of acute experimental allergic encephalomyelitis, and (3) inhibition is also present when treatment is begun after sensitization, suggesting an effect of prolactin on the effector limb of the immune response during experimental allergic encephalomyelitis.
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PMID:The role of prolactin in autoimmune demyelination: suppression of experimental allergic encephalomyelitis by bromocriptine. 158 47

We examined the effect of bromocriptine (BCR) treatment on the duration and severity of neurological symptoms of acute experimental allergic encephalomyelitis (EAE), an animal model for demyelinating diseases, particularly multiple sclerosis. To mimic the clinical situation, BCR treatment was started after the onset of clinical signs. Furthermore, the effect of BCR treatment on the course of a chronic relapsing form of EAE was studied. BCR was injected at daily intervals in a dose that resulted in sustained suppression of plasma concentrations of prolactin, a pituitary hormone that plays a role in immunoregulation. In acute EAE, BCR therapy reduced both severity and duration of the clinical signs. In chronic relapsing EAE, BCR treatment did not affect the severity and duration of the first attack, but reduced the duration of the subsequent, second attack. Thus, BCR treatment improves the clinical course in animals with ongoing disease. These findings may have implications for the search for new therapeutic approaches in multiple sclerosis.
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PMID:Therapeutic effect of the D2-dopamine agonist bromocriptine on acute and relapsing experimental allergic encephalomyelitis. 819 Aug 33

The effect of dihydroergocryptine, a natural alkaloid derivative which exhibits D2 dopaminomimetic properties, has been studied in Lewis female rats with experimentally induced allergic encephalomyelitis. A chronic treatment with dihydroergocryptine started two days before immunization, induced a dramatic reduction of prolactin levels accompanied by a marked amelioration of neurological signs. In addition, the proliferative activity of splenic lymphocytes induced by the mitogen Concanavalin-A (Con-A) was reduced in dihydroergocryptine-treated animals. It is suggested that this effect is related to the ability of dihydroergocryptine to lower prolactin concentrations or also, partially, to a neuroprotective action of this drug.
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PMID:Dihydroergocryptine protects from acute experimental allergic encephalomyelitis in the rat. 840 36

Prolactin is essential for immune function. Excess prolactin augments some immune reactions, whereas low serum levels of prolactin inhibit immune function and prevent experimental allergic encephalomyelitis, an animal model of multiple sclerosis (MS). Activated lymphocytes, characteristics of MS, release prolactin. In this study, serum prolactin levels were normal in 35 patients with chronic progressive MS and 19 patients with acute exacerbations. These results suggest it is unlikely that prolactin contributes to the enhanced immune reactivity characteristic of MS. Acute cyclosporin A (CsA) administration increases circulating prolactin levels in animals and might paradoxically augment some immune reactions. We find that chronic CsA therapy for MS does not cause elevations in serum prolactin and should not reverse any therapeutic effect of CsA. Disturbances of prolactin regulation are not characteristic of MS.
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PMID:Serum prolactin levels in active multiple sclerosis and during cyclosporin treatment. 841 56

Multiple sclerosis (MS) is a human disease characterized by chronic demylination in the brain caused by immunological mechanisms involving T lymphocytes and macrophages. Recently developed models of chronic relapsing forms of experimental allergic encephalomyelitis, sharing many of the clinical and pathological features of MS, and new discoveries of efficient autoregulatory mechanisms intrinsic to the immune system, have suggested new possibilities for therapeutic intervention in MS. Moreover, recent data support the concept that the immune system is exposed to a broad framework of regulation, including neuroendocrine control. In particular, interfering with secretion of the lactogenic hormone prolactin and of glucocorticoids has consistently resulted in a reduction of clinical and pathological manifestations of the disease. In this review, Frank Berkenbosch and colleagues highlight several of the possible therapeutic opportunities for the treatment of MS.
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PMID:Multiple sclerosis: some possible therapeutic opportunities. 851 55

Before the onset and during experimental allergic encephalomyelitis (EAE), the animal counterpart of multiple sclerosis (MS), prolactin levels were found to be elevated and bromocriptine was found to attenuate the attacks. This study was designed to determine whether patients with MS show evidence of hyperprolactinemia. Twelve patients with MS and twelve healthy controls were studied at baseline and with TRH stimulation, a provocative test for prolactin secretion. Compared to matched controls, patients with MS had slightly but significantly higher prolactin levels at baseline (10.2+/-1.6 vs 6.4 4+/-0.57 ng/ml, P=0.042), however, values were within the normal range. The prolactin levels post TRH were significantly higher in patients with MS: peak prolactin level was higher in patients than controls (57.08+/-6.144 vs 32.94+/-4.92 ng/ml, P=0.006). The area under the curve of prolactin was also higher in patients than in controls (3421.87+/-394.53 vs 2317.62+/-257.22 ng/ml, P=0.030). These findings are compatible with data from studies of experimental animals with MS and suggest that prolactin may play a role in the immunology of MS.
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PMID:Prolactin secretion is increased in patients with multiple sclerosis. 1038 82

Prolactin receptors were identified on the membranes of lymphocytes have been demonstrated to secrete prolactin. The decrease, as well as the increase of the prolactin level in the plasma are responsible for immune disorders. Prolactin dysfunction has been described in some autoimmune diseases, such as systemic lupus erythematosus, immune arthritis, uveitis, experimental allergic encephalomyelitis and thyroid disease. The normal prolactin secretion is trophic for the lymphocytes, while the high and also the low levels of prolactin may play an immunosuppressive role.
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PMID:Prolactin secretion and the immune system. 1075 71

Leptin is 16 kDa adipokine that links nutritional status with neuroendocrine and immune functions. Initially thought to be a satiety factor that regulates body weight by inhibiting food intake and stimulating energy expenditure, leptin is a pleiotropic hormone whose multiple effects include regulation of endocrine function, reproduction, and immunity. Leptin can be considered as a pro-inflammatory cytokine that belongs to the family of long-chain helical cytokines and has structural similarity with interleukin-6, prolactin, growth hormone, IL-12, IL-15, granulocyte colony-stimulating factor and oncostatin M. Because of its dual nature as a hormone and cytokine, leptin links the neuroendocrine and the immune system. The role of leptin in the modulation of immune response and inflammation has recently become increasingly evident. The increase in leptin production that occurs during infection and inflammation strongly suggests that leptin is a part of the cytokine network which governs the inflammatory-immune response and the host defense mechanisms. Leptin plays an important role in inflammatory processes involving T cells and has been reported to modulate T-helper cells activity in the cellular immune response. Several studies have implicated leptin in the pathogenesis of autoimmune inflammatory conditions, such as experimental autoimmune encephalomyelitis, type 1 diabetes, rheumatoid arthritis, and intestinal inflammation. Very recently, a key role for leptin in osteoarthritis has been demonstrated: leptin indeed exhibits, in concert with other pro-inflammatory cytokines, a detrimental effect on articular cartilage by promoting nitric oxide synthesis in chondrocytes. Here, we review the recent advances regarding leptin biology with a special focus on those actions relevant to the role of leptin in the pathophysiology of inflammatory processes and immune responses.
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PMID:Leptin, from fat to inflammation: old questions and new insights. 1564 35

This work analyzes the effect of calorie restriction on the development of experimental allergic encephalomyelitis (EAE) in Lewis rats. Plasma levels of ACTH, corticosterone, prolactin and growth hormone (GH) and mitogenic responses in submaxillary lymph nodes were measured. Male Lewis rats (6 weeks-old) were submitted to a calorie restriction equivalent to 66% of food restriction or to a normal diet. Fifteen days later, rats were injected with complete Freund's adjuvant plus spinal chord homogenate (SCH) or with complete Freund's adjuvant alone. Rats were monitored daily for clinical signs of EAE and were killed on day 15 after immunization. Only rats subjected to normal diet exhibited clinical signs of the disease. The increase in plasma ACTH and corticosterone found after SCH immunization in controls was not detectable in calorie restricted rats. Likewise, the correlation between circulating ACTH and corticosterone was no longer found after calorie restriction. Generally, calorie restriction by itself augmented plasma ACTH or corticosterone and this increase was not further amplified by SCH immunization. Only calorie restricted rats exhibited augmented plasma prolactin levels after SCH immunization, and decreased plasma GH levels regardless of immunization. Calorie restriction depressed the mitogenic response of lymphoid cells to concanavalin A but not to lipopolysaccharide. Calorie restricted rats did not exhibit augmented mitogenic response to concanavalin A following SCH immunization as those found in controls. The results are compatible with the view that the course of EAE can be significantly modified by caloric restriction.
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PMID:Experimental allergic encephalomyelitis in male Lewis rats subjected to calorie restriction. 1595 42

Treatment of susceptible rats with dopaminergic agonists that reduce prolactin release decreases both severity and duration of clinical signs of experimental allergic encephalomyelitis (EAE). To assess to what extent the presence of an ectopic pituitary (that produces an increase in plasma prolactin levels mainly derived from the ectopic gland) affects EAE, 39 male Lewis rats were submitted to pituitary grafting from littermate donors. Another group of 38 rats was sham-operated by implanting a muscle fragment similar in size to the pituitary graft. All rats received subcutaneous (s.c.) injections of complete Freund's adjuvant (CFA) plus spinal cord homogenate (SCH) and were monitored daily for clinical signs of EAE. Animals were killed by decapitation on days 1, 4, 7, 11 or 15 after immunization and plasma was collected for prolactin RIA. In a second experiment, 48 rats were immunized by s.c. injection of a mixture of SCH and CFA, and then received daily s.c. injections of bromocriptine (1 mg/kg) or saline. Groups of 8 animals were killed on days 8, 11 or 15 after immunization and plasma prolactin was measured. Only sham-operated rats exhibited clinical signs of the disease when assessed on day 15 after immunization. A progressive decrease in plasma prolactin levels was observed in pituitary-grafted rats, attaining a minimum 15 days after immunization, whereas plasma prolactin levels were increased during the course of the disease in sham-operated rats. Plasma prolactin levels were higher in pituitary-grafted rats than in sham-operated rats 1 day after immunization, but lower on days 7, 11 and 15 after immunogen injection. Further supporting a correlation of suppressed prolactin levels with absence of clinical signs of EAE, rats that were administered the dopaminergic agonist bromocriptine showed very low plasma prolactin levels and did not exhibit any clinical sign of EAE. These results indicate that low circulating prolactin levels coincide with absence of clinical signs of EAE in Lewis rats.
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PMID:Experimental allergic encephalomyelitis in pituitary-grafted Lewis rats. 1692 63


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