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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental allergic encephalomyelitis (EAE) was induced in rabbits by inoculation of homologous spinal cord myelin with Freund's adjuvant. During the paralytic stage of EAE rabbits were injected with 2-C14-acetate and sacrificed in two hours. As revealed, the intensity of phospholipid and cholesterol synthesis decreased markedly in rabbits with EAE not only in the lumbar part of the spinal cord (where the greatest lesions of myelin were localized), but also in the brain stem (where demyelinization was absent).
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PMID:[Intensity of phospholipid and cholesterol synthesis in the brain and spinal cord of rabbits with experimental allergic encephelomyelitis]. 95 70

In rabbits the acute form of experimental allergic encephalomyelitis was caused by inoculation of emulsion of homologous myelin from spinal cord with Freund's adjuvant. In terminal paralytic period of the disease the animals were subcutaneously administered with 2-14C-acetate and a dose 50 micronCi per 100 g of body weight 2 hrs before death. From lumbar and stem sections of the central nervous system purified fractions of cerebrosides and gangliosides were isolated and their specific radioactivity was determined. The intensity of the cerebrosides synthesis was found to be distinctly decreased not only in the more impaired lumbar region but also in the stem section of the central nervous system, where the centers of demyelinization were not observed. The intensity of the gangliosides synthesis was also markedly decreased, in spite of that their content was not altered in the central nervous system under experimental allergic encephalomyelitis.
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PMID:[Intensity of incorporation of 2-C14-acetate into the cerebrosides and gangliosides of the brain and spinal cord of rabbits in experimental allergic encephalomyelitis]. 102 74

A bitch was inoculated subcutaneously and intramuscularly with Neospora caninum tachyzoites on Day 35 of pregnancy. Eight pups were born 28 days later. Five pups became ill and necropsies were performed before 20 days of age. Three pups and the bitch remained clinically normal for 7 weeks after parturition when they were intramuscularly injected with 40 mg kg-1 methylprednisolone acetate weekly to activate chronic N. caninum infection. Necropsies were performed 48, 17, 18, and 18 days respectively after administration of corticosteroids. Hepatic necrosis, pneumonia, encephalomyelitis, and myonecrosis were the main changes seen in these dogs.
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PMID:Neosporosis in dogs. 238 83

The treatment of Lewis rat peritoneal macrophages with p1-nitrophenyl p-guanidinobenzoate (NPGB) inhibited the superoxide anion production stimulated with phorbol myristate acetate (PMA). The addition of NPGB at the time of maximum superoxide generation was still able to block the superoxide release. It appears from these findings that NPGB may block either the activation process of the membrane bound NAD(P)H oxidase or directly on the active enzyme. Other protease inhibitors such as, epsilon-amino caproic acid (EACA), pepstatin, trans aminomethyl cyclohexane carboxylic acid (AMCA), aprotinin, and leupeptin did not inhibit the superoxide release. The superoxide anion release by the xanthine-xanthine oxidase system was not inhibited by NPGB. This finding indicates that NPGB does not itself react with superoxide. It has been also demonstrated that NPGB is a good reactant toward sulfhydryl group. The relevance of these finding to experimental allergic encephalomyelitis (EAE) is discussed.
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PMID:NPGB-induced inhibition of superoxide anion production by normal Lewis rat macrophages. 254 Apr 44

In most demyelinating diseases, macrophages are believed to be active agents of myelin destruction. In experimental encephalomyelitis, these cells appear to strip off and ingest the myelin lamellae, and myelin debris has been observed within the cell body. We show here in vitro conditions in which rat peritoneal macrophages phagocytose and metabolize CNS myelin lipids. Purified rat myelin, prelabeled in vivo with [14C]acetate, was incubated with preimmune serum or rabbit antiserum to rat CNS myelin and added to macrophage monolayers. Myelin opsonized with antimyelin antibodies was more readily phagocytosed and metabolized by cultured macrophages than untreated myelin or that preincubated with preimmune serum. In the presence of macrophages, levels of myelin polar lipids and cholesterol decreased, whereas radioactive cholesterol ester and triglyceride accumulated. Up to five times as much radioactive cholesterol ester and about twice as much triglyceride accumulated in macrophage cultures containing antibody-treated myelin as in cultures fed preimmune serum-treated myelin or in those incubated with untreated myelin. Both the fatty acid and the cholesterol from cholesterol ester contained radioactive label; therefore, both were derived at least partly from the radioactive myelin lipid. Antiserum to myelin purified from peripheral nerve was almost as effective as that to CNS myelin in stimulating cholesterol metabolism, whereas antiserum to galactocerebroside was about 70% as active. Antiserum to basic protein had less effect, whereas antiserum to the myelin-associated glycoprotein and proteolipid protein was inactive. Of the polar lipids, ethanolamine phosphatide was most degraded in both the antiserum- and preimmune serum-treated myelin, with the diacyl form and plasmalogen form degraded about equally. These experiments indicate that myelin-specific antibodies in inflammatory CNS lesions may participate in and stimulate macrophage-mediated demyelination.
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PMID:Opsonization with antimyelin antibody increases the uptake and intracellular metabolism of myelin in inflammatory macrophages. 373 1

Experimental allergic encephalomyelitis (EAE) was induced in female rats and a comparison of the effects of melengestrol acetate (MGA) and hydrocortisone acetate (HCA) was made. A dose response relation was observed. 2-4 mg MGA/kg/day delayed onset of the disease and 16 mg/kg/d ay for 19 days completely inhibited the disease. 20 mg HCA was comparable to 2-4 mg MCA in effectiveness. To determine if MCA or HCA could arrest or reverse the established disease, 25 mg MCA/kg or 125 mg HCA/kg were administered weekly beginning between 7 and 24 days postsensitization. When dosing was started up to 16 days postsensitizat ion, MGA was more effective than HCA, however when started at 24 days, little difference between the 2 was noted. Some reversal of disease was noted when a single dose of MCA (100 mg/kg) or HCA (500 mg/kg) was given 16, 20 or 24 days postsensitization. It was concluded that both MGA and HCA prevented the development of EAE and reversed the established disease. MCA was considered superior to HCA in both prophylactic and therapeutic treatment.
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PMID:A comparison of the effects of melengestrol acetate and hydrocortisone acetate on experimental allergic encephalomyelitis in rats. 544 6

Cerebrospinal fluid (CSF) was taken from strain 13 guinea pigs in various stages of chronic relapsing experimental allergic encephalomyelitis, the spinal cords removed for histological examination and meningeal stretch preparations made. CSF cells were counted and characterized by morphological studies, anti-IgG and alpha-naphthyl acetate esterase (ANAE) staining. Approximately 65% of normal CSF lymphocytes were ANAE positive and 10% stained with anti-IgG. No polymorphonuclear leucocytes were seen. Five out of eight relapsing animals had raised cell counts (up to 152/microliters) as did three animals in remission. There was no change in the proportion of various types of CSF cells where increased numbers were recorded. Infiltrating cells in spinal cord sections and meningeal preparations were similarly characterized and the results compared with CSF cells findings. Animals in relapse which had, in addition, macroscopically visible cord plaques showed the most severe infiltrative changes in spinal cord tissue and in the meninges. There were differences between the proportion of various types of CSF cells and meningeal infiltrate cells on ANAE staining reaction. In general there were far more lymphocyte-type cells in the CSF but more monocyte-type cells in meningeal infiltrates.
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PMID:Chronic relapsing experimental allergic encephalomyelitis: cerebrospinal fluid cytology and a comparison with meningeal and spinal cord pathology. 687 20

During experimental allergic encephalomyelitis (EAE), both blood-borne macrophages as well as activated, resident microglial cells are considered to be involved in inflammatory reactions in the central nervous system (CNS), resulting in the neurological deficits common to EAE. Both cell types can produce multiple mediators of tissue damage, among which are the reactive oxygen species (ROS). In this study we show that macrophages and microglial cells, isolated from the CNS of Lewis rats with clinical signs of EAE, exhibited significantly elevated spontaneous and phorbol myristate acetate (PMA)-inducible levels of ROS compared to similar cells isolated from healthy controls, sham (complete Freund's adjuvant, CFA)-immunized rats as well as rats sacrificed before the manifestation of clinical signs of EAE. However, during clinical EAE, peripheral blood mononuclear cells (PBMC) did not show increased spontaneous nor PMA-inducible ROS production compared to controls. In vivo treatment of EAE with catalase, which scavenges the ROS H2O2, markedly suppressed the severity of the disease as compared to sham (albumin)-treated controls. In contrast, superoxide dismutase had no effect on clinical signs. Our studies point at a putative functional role for ROS, and in particular H2O2, in the pathogenesis of EAE.
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PMID:Reactive oxygen species are involved in the pathogenesis of experimental allergic encephalomyelitis in Lewis rats. 786 Jul 16

Peripheral macrophages infiltrating the central nervous system and resident microglia phagocytize myelin in cell-mediated demyelinating diseases, including experimental autoimmune encephalomyelitis and multiple sclerosis. A cascade of cytokines is believed to modulate the immunological sequence of events occurring in these conditions, and several of these mediate their effects through the protein kinase C pathway. Therefore, we compared the effects of phorbol myristate acetate (PMA), an activator of protein kinase C, on various functions of cultured macrophages and microglia. PMA at moderate concentrations induced apoptosis in macrophages, and this process appeared to be increased in the presence of myelin. In contrast, microglia were activated by PMA, and greatly increased their phagocytosis of myelin. Control macrophages released a considerable amount of proteolytic activity into the medium, as measured by the breakdown of myelin basic protein, and in the process of undergoing apoptosis from PMA-treatment, even higher amounts were released. The enzyme activity in control macrophage medium was inhibited mainly by PMSF and calpain inhibitors, while that from PMA-treated macrophages was inhibited by calpain inhibitors only. An ICE inhibitor was ineffective in inhibiting activity in medium from PMA-treated cells undergoing apoptosis. Medium from microglia contained very little proteolytic activity, and this was not increased by PMA. Cultured macrophages showed little evidence of oxygen free radical release as measured by the TBARS procedure, and PMA had no effect. Microglia, on the other hand, produced higher levels of reactive oxygen species, with a further increase of 18% by PMA. Thus major functions of these phagocytic cells appear to be modulated by the protein kinase C pathway, although the two cell types show very different responses to an activator of this signal.
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PMID:Effects of phorbol myristate acetate (PMA) on functions of macrophages and microglia in vitro. 948 57

The underlying pathophysiology of multiple sclerosis is presumed to be autoimmune in nature. Attempts to find an effective treatment for this common disease of the central nervous system have primarily focused on immune-mediated therapies, both immunosuppressive and immunomodulatory. The wide variety of immunological abnormalities detected in multiple sclerosis and its animal model, experimental allergic encephalomyelitis, has prompted the testing of a diverse array of drugs to be used for treatment. Recent successes in the treatment of relapsing-remitting multiple sclerosis with interferon beta and glatiramer acetate have renewed interest in and raised expectations for the effective control of this neurological disorder. Improved methodology in clinical trials, the development of surrogate markers and the availability of novel therapies bode well for more rapid advances.
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PMID:Current immunotherapy in multiple sclerosis. 955 77


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