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)

Although T cell receptor (TCR) peptide therapy was initially reported to be a very effective method for prevention of the development of experimental autoimmune encephalomyelitis (EAE), it was recently demonstrated that the same peptide immunization led to enhanced and chronic EAE in some cases. In the present study, we examined the effect of the TCR peptide (V beta 8.2-39-59) vaccination on the development of EAE by employing several immunization protocols. We found that TCR peptide vaccination effectively prevented EAE development only when the peptide was injected with Mycobacterium tuberculosis-enriched CFA in the vicinity of the challenge site. Under such conditions, a sufficient number of peptide-reactive T cells were generated. Flow cytometry and immunohistochemical analyses using anti-peptide antibody and anti-V beta 8.2 mAb revealed that despite the presence of V beta 8.2+ cells, very few peptide-positive T cells appeared in the lymphoid organs throughout the course of EAE. These findings imply that antibodies that are generated after immunization with V beta 8P are hardly accessible to their specific epitopes in the native protein. Insufficient generation of both T cells and antibodies against V beta 8.2-positive T cells may be attributable to the outcome of the therapy. To establish effective TCR peptide immunotherapy, these disadvantages should be overcome by using other TCR sequences and/or by employing a more suitable adjuvant.
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PMID:T cell receptor peptide therapy for autoimmune encephalomyelitis: stronger immunization is necessary for effective vaccination. 811 76

We induced a chronic relapsing form of experimental autoimmune encephalomyelitis in 7- to 10-week-old female SJL/J mice using a subcutaneous injection of an emulsion containing syngeneic mouse spinal cord homogenate in phosphate-buffered saline and Mycobacterium tuberculosis (MT) in incomplete Freund's adjuvant. Following the animals' recovery from the first attack periods, we fed them varying doses of type I interferon (IFN) or mock IFN three times per week for 6 weeks. This treatment decreased proliferation to guinea pig myelin basic protein and MT compared with control in draining lymph node and diminished inflammation in the CNS. Oral IFN altered the cytokine profile of concanavalin A-activated spleen cells by decreasing IFN-gamma secretion. These results suggest that type I IFNs are active by the oral route, have significant clinical and immunomodulatory effects, and can decrease an established and ongoing immune response to sensitized antigens. The oral administration of biologic-response modifiers, such as type I IFNs, provides a potentially nontoxic, convenient, continuous means of delivering immunoactive substances via the gut regional immune system that can alter cytokine production and suppress clinical relapses.
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PMID:Suppression of relapsing experimental autoimmune encephalomyelitis in the SJL/J mouse by oral administration of type I interferons. 820 13

Chronic relapsing experimental allergic encephalomyelitis, an animal model of multiple sclerosis, was induced in Strain 13 guinea-pigs by subcutaneous injection of spinal cord homogenate and Freund's incomplete adjuvant supplemented with Mycobacterium tuberculosis. High resolution 1H NMR spectra of CNS tissue extracts indicated that the levels of choline metabolites, particularly betaine, were elevated in the spinal cord tissue, the principal site of lesion formation in this guinea-pig strain. The spectra also show that N-acetylated compounds are slightly depleted in the disease. The results are discussed in relation to the biochemical interpretation of NMR spectra obtained in vivo from patients with multiple sclerosis.
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PMID:Experimental allergic encephalomyelitis raises betaine levels in the spinal cord of strain 13 guinea-pigs. 834 53

Treatment of SJL mice with 400 ng Bordetella pertussis toxin (PT) either in saline or emulsified in incomplete Freund's adjuvant protected the mice against experimental autoimmune encephalomyelitis (EAE) induced 28 days later by a synthetic peptide of myelin proteolipid protein (PLP139-151) in complete Freund's adjuvant. However, treatment with a genetically inactivated pertussis toxin in which the catalytic and NAD-binding sites of the ADP-ribosyltransferase subunit were modified by site-directed mutagenesis was without effect. In vitro, lymphocyte proliferation was considerably enhanced by both the native and the inactivated toxin, at concentrations of 0.1-1 microgram/ml. However, strong inhibition of proliferation was also observed with the native toxin only, at concentrations that were two to three orders of magnitude lower than that required for the mitogenic effect (0.1-1 ng/ml). The inhibition of proliferation was detectable in the case of high-background proliferation, after stimulation with antigen (PLP139-151) or purified protein derivative of Mycobacterium tuberculosis), or with anti-CD3 monoclonal antibody, but not after stimulation with concanavalin A or phorbol esters and Ca2+ ionophore. These results suggest that the inhibitory effect of PT operates by interfering selectively with a T cell receptor-dependent signaling pathway. The biological significance of the in vitro inhibitory effect of PT was demonstrated by a considerable decrease and/or delay in the ability of lymphocytes grown with PLP139-151 and low concentrations of PT to transfer EAE to naive recipients.
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PMID:Native, but not genetically inactivated, pertussis toxin protects mice against experimental allergic encephalomyelitis. 864 Aug 62

The present study sought to examine the immunopharmacologic effects of suramin on splenocytes from experimental allergic encephalomyelitis (EAE)-induced mice, taken in line with a previous observed action of suramin in ameliorating EAE. Suramin, a polysulfonated napthylurea, decreased the proliferation of T cells, in the presence of various stimuli, such as guinea pig myelin basic protein (MBP), mouse spinal cord homogenate (MSCH), bovine proteolipid protein (PLP), P1 (synthetic peptide 139-151 of PLP), and Mycobacterium tuberculosis (MTB). Suramin inhibited T cell proliferation in a dose-dependent manner. However, cytokine assays revealed that suramin increased antigen-induced levels of IL-4, whilst IFN-gamma levels were decreased. Using various doses of suramin (25, 15, and 5 micrograms/g), its cytokine modulatory effect displayed a consistent dose-dependent activity in vivo. This cytokine modulation commenced on week 2 after immunization and persisted all throughout the drug administration period, up to the 4th week. These results indicate that the prospects of using suramin in the treatment of multiple sclerosis may be feasible.
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PMID:Suramin exerts in vivo cytokine modulatory properties on splenocytes from experimental allergic encephalomyelitis-induced SJL mice: implications for autoimmune disease therapy. 895 79

From 1992 to mid-1996, a national survey of poultry diseases in Lebanon was conducted. This surveillance included meat breeder, layer breeder, commercial layer and chicken broiler flocks. The history, signs, lesions and laboratory tests of poultry were used in the diagnosis of prevalent poultry diseases. Culture techniques were used to screen for bacterial diseases; serological techniques and, to a lesser extent, culture techniques were used to diagnose viral diseases; and both serological and culture techniques were used to diagnose Mycoplasma infections. The outbreaks of diseases detected in broiler breeder flocks and the number of such flocks experiencing these diseases were as follows: femoral head necrosis (6), egg-drop syndrome (3), reovirus-associated malabsorption syndrome (3), synovitis (Mycoplasma synoviae infection) (7), swollen head syndrome (SHS) (3), tenosynovitis (viral arthritis) (1), lymphoid leukosis (3), avian encephalomyelitis (1), fowl pox (1) and aortic rupture (1). The disease outbreaks detected in layer breeders were as follows: SHS (2), bumble foot (2), egg-drop syndrome (3) and avian infectious bronchitis (IB) (1). The disease outbreaks detected in commercial layer flocks were as follows: egg-drop syndrome (5), avian infectious laryngotracheitis (2), avian IB (nephrogenic strain) (1), malabsorption (1), avian tuberculosis (Mycobacterium avium) (1), Marek's disease (1), fowl pox (1), Salmonella enterica subsp. enterica Enteritidis infection (1), salpingitis (1) and Heterakis gallinae infestation (1). The disease outbreaks detected in broiler flocks were as follows: colibacillosis (40), infectious bursal disease (Gumboro disease) (15), malabsorption syndrome (8), avian infectious laryngotracheitis (8), paratyphoids (salmonellosis) (7), femoral head necrosis (8), SHS (6), avian mycoplasmosis (Mycoplasma gallisepticum infection) (6), synovitis (7), avian IB (6), botulism (1), avian encephalomyelitis (1) and gangrenous dermatitis (1). Diseases which occurred and which were reported for the first time in Lebanon were as follows: bumble foot, femoral head necrosis, avian IB (nephrogenic strain), malabsorption syndrome and SHS. This surveillance helped to establish baseline data concerning the predominant poultry diseases in Lebanon. Such information is a prerequisite for future regional and international collaboration to identify the source of the aetiological agents and to control their spread to neighbouring countries.
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PMID:National surveillance of poultry diseases in Lebanon. 956 2

An interesting neurological syndrome, characterized by recurrent optic neuritis, cervical myelopathy from syringomyelia, paraparesis, amenorrhea-galactorrhea, and other endocrine problems, has been described among young black women in the French West Indies. The etiology remains unknown, but possible links with Devic's disease, acute disseminated encephalomyelitis, and neurotoxicity from quinolines in Annona muricata teas have been postulated. The largest epidemic of neuropathy in this century occurred in Cuba in 1991-1994. Clinical features and etiologic studies are reviewed. Its primary cause was nutritional. A similar epidemic was recently described in Tanzania. A number of infectious neuropathies and myopathies are reviewed, including leprosy, tuberculosis, hemorrhagic fevers (Ebola and Marburg filoviruses, Lassa, Argentinean and Bolivian arenaviruses), the human retrovirus human T-cell lymphotropic virus type I, Lyme disease and postimmunization neuropathies. The tropics continue to contribute interesting and important clinical conditions that may illuminate the etiopathiogenesis of other common disorders.
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PMID:Tropical myeloneuropathies revisited. 984 4

A herbal formula, Badmaev 28, was evaluated in the treatment of an induced attack in a chronic relapsing model of experimental allergic encephalomyelitis (EAE) in SJL/J mice. Chronic EAE was induced by immunization of 8 week old mice with an emulsion of syngeneic spinal cords with incomplete Freund's adjuvant supplemented with Mycobacterium tuberculosis. Therapy with Badmaev 28 was started on day 25 after the immunization, and the formula was administered in the drinking water at doses of 7, 21, 83 and 166 mg/kg/day. The treatment resulted in significantly decreased mortality compared with the untreated control animals and the therapeutic effect occurred in one experiment in a dose-dependent fashion. Based on the experimental results it is difficult to name one particular mechanism responsible for the therapeutic effectiveness of the formula in the EAE model. Rather this protective effect could be explained by a broad protective mechanism of action discussed in the literature as nonspecific resistance (NSR) to the diversified biological and psychological stressors. The increase in NSR characterizes the action of pharmacological compounds termed adaptogens or bioprotectants.
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PMID:The therapeutic effect of an herbal formula Badmaev 28 (padma 28) on experimental allergic encephalomyelitis (EAE) in SJL/J mice. 1035 61

We report that SJL mice developed chronic relapsing experimental autoimmune encephalomyelitis (CR-EAE) when injected with a mixture of mouse spinal cord homogenate (MSCH), killed mycobacteria tuberculosis (M. tb), and mycobacteria butyricum (M. b) in PBS 2 months before a conventional acute experimental autoimmune encephalomyelitis (EAE) induction injection. The altered progression of the disease involved an accelerated but less severe acute attack and development of a chronic course with relapsing-remitting episodes. Histological examination revealed inflammatory cell infiltration and demyelination in the brain. The dose of neuroantigen as well as the anatomical sites of injections were found to be crucial for the development of the disease.
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PMID:A novel and efficient regimen for producing chronic relapsing experimental autoimmune encephalomyelitis (CR-EAE) in SJL mice. 1051 31

Previous studies demonstrated that blood-brain barrier (BBB) breakdown observed at the cerebral level during experimental allergic encephalomyelitis (EAE) arises from the presence of Mycobacterium tuberculosis in Freund's adjuvant and not only from the encephalitogenic antigens. The main objective of this study was to check if the mannan moiety of lipoarabinomannan present in the mycobacterial cell envelope is responsible for an immune response provoking a BBB breakdown. The results showed that: firstly, the complete Freund's adjuvant (CFA) contains a high release of polysaccharides; secondly, the rats immunized with the CFA present important serum concentration of anti-mannan antibody; and finally, a single 2-mg dose of anti-mannan antibody injected intravenously in naive rats provokes an immediate and reversible BBB breakdown. These results suggest that mannan arising from the solubilization of the mycobacterial cell wall in Freund's adjuvant induces a high production of anti-mannan antibody, which, in turn, provokes a BBB breakdown and possibly facilitates the induction of EAE.
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PMID:Antibody directed against mannan of the Mycobacterium tuberculosis cell envelope provokes blood-brain barrier breakdown. 1067 90


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