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

Experimental autoimmune encephalomyelitis (EAE) is a cell-mediated autoimmune disease of the central nervous system that has been extensively studied in the rat. The Lewis rat is highly susceptible to the induction of EAE, while the Lewis resistant (LeR) rat is known to be resistant. In this paper, we demonstrate that the LeR rat, which was derived from the Lewis strain by inbreeding of fully resistant animals, is histocompatible with the Lewis strain. Radiation chimeras, a tool for distinguishing between immunologic and nonimmunologic resistance mechanisms, were utilized to analyze the cellular mechanisms involved in genetic resistance to EAE. By transplanting bone marrow cells from LeR rats into irradiated Lewis recipients, Lewis rats were rendered resistant to EAE induction. Likewise, transplanting Lewis bone marrow cells into irradiated LeR recipients rendered LeR rats susceptible. Mixed lymphoid cell chimeras using bone marrow, spleen, and thymus cells in Lewis recipient rats revealed individual lymphoid cell types and cell interactions that significantly affected the incidence and severity of EAE. Our results suggest that LeR resistance is mediated by hematopoietic/immune cells, and that cells located in the spleen appear to play a critical role in the resistance/susceptibility to EAE induction. Depletion of splenic adherent cells did not change the patterns of EAE resistance. In vivo cell mixing studies suggested the presence of a suppressor cell population in the LeR spleen preparations which exerted an inhibitory effect on Lewis autoimmune responses. Thus, the mechanism of LeR resistance appears to be different from that in other EAE-resistant animals.
 ...
PMID:Genetic resistance in experimental autoimmune encephalomyelitis. I. Analysis of the mechanism of LeR resistance using radiation chimeras. 252 17

Oral administration of spirogermanium (Sg), inhibits the development of immune-mediated hindpaw inflammation in the rat model of adjuvant arthritis (AA) and DTH responses to PPD (30 mg/kg/day). A similar dosing protocol inhibits hindleg paralysis in experimental autoimmune encephalomyelitis (EAE). The spleens of these animals and those of normal rats contain radiation resistant (2000 R) non-specific suppressor cells (SC) which bear some similarity to those generated following total lymphoid irradiation (TLI). These cells do not appear to be mature T cells, they are partially adherent to plastic, sephadex G10 and nylon wool, insensitive to indomethacin and are enriched in a 1.07 g/ml fraction of a Percoll density gradient.
 ...
PMID:Inhibition of autoimmune disease and the generation of suppressor cells by spirogermanium: a biological profile similar to total lymphoid irradiation. 252 42

Intranasal (i. n.) infection with 10 LD50 of Sindbis virus caused acute encephalomyelitis and death in ABD2F1 mice 3-7 days post infection (p.i.). Histologic lesions were found in the CNS, pancreas. liver, parotid glands, exorbital lacrimal glands, lymphoid organs and kidneys. Repeated oral administration of the anticholinergic anti-Parkinson drug Norakin protected infected animals from death in a dose-dependent manner when treatment was started prior to but not after virus inoculation. The maximum protective effect was achieved when the drug was administered twice daily at doses of 2.5 or 5.0 mg/kg body mass for at least 56 hr; single injections of the full daily dose were ineffective. Daily doses of greater than or equal to 25 mg/kg body mass had a reduced protective effect or failed to prevent mortality. Administration of Norakin up to doses of 300 mg/kg body mass per day to noninfected ABD2F1 mice were tolerated without obvious clinical or histological signs of illness over a period of 104 hr. Replication of sindbis virus in BHK 21/C13 cells was not inhibited by Norakin concentrations up to 10 micrograms/ml. In Mengo virus-infected mice Norakin did not exert any protective effect within the range of 1.25-50.0 mg/kg body mass when treatment started 1 hr before infection and has been continued twice daily over a period of 104 hr.
 ...
PMID:Inhibition by Norakin (triperiden) of Sindbis virus infection in mice. 286 21

In this study, pretreatment of Lewis rats with a syngeneic encephalitogenic T cell line (S1) was found to be able to constantly induce resistance to the subsequent induction of transferred experimental autoimmune encephalomyelitis (tEAE). This treatment was capable of protecting recipient animals for at least 2-4 months. Here we show an enhanced suppressor T(anti-S1) cell activity, which can be readily detected in the lymphoid organs of animals which recovered from S1-induced tEAE, or from rats pretreated with attenuated (irradiated, fixative treated or water-lysed) S1 cells. Anti-S1 cells, which uniformly express the CD8 phenotype, were selectively stimulated to grow and expand into lines by confronting primed lymphoid cells with irradiated S1 cells in culture. The proliferative response of anti-S1 cells was independent of myelin basic protein and antigen-presenting cells, and the responses against unrelated encephalitogenic T cell lines were minimal. It was also found that none of the monoclonal antibodies tested (including CD8 and MHC class I antigen-specific antibodies) was able to block S1/anti-S1 interactions. These cells are functionally suppressive to the proliferation of S1 cells in vitro, are specifically cytolytic directed against the EAE-inducing S1 cells and are able to antagonize encephalitogenic capacity of S1 cells in vivo. In vivo elimination of the CD8+ T subset from Lewis rats, using a combined treatment of thymectomy and OX-8 antibody injection before the initial cell transfer, totally blocked the induction of resistance. Our experiments document that induction of functionally active suppressor T cells is responsible for the induced resistance observed in tEAE.
 ...
PMID:Regulatory circuits in autoimmunity: recruitment of counter-regulatory CD8+ T cells by encephalitogenic CD4+ T line cells. 290 95

Cultures of myelinated SJL/J fetal mouse spinal cord were incubated with serum and lymphoid cells from syngeneic animals with experimental allergic encephalomyelitis (EAE) induced by syngeneic spinal cord homogenate (SSCH) in complete Freund's adjuvant or others injected with complete Freund's adjuvant alone. After 24 or 48 h of exposure, demyelination was determined by light microscopic examination and quantification of 2',3'-cyclic nucleotide 3'-phosphohydrolase activity. Cultures exposed to spleen or lymph node cells from SSCH-sensitized animals showed the greatest alterations in myelin and decreases in 2',3'-cyclic nucleotide 3'-phosphohydrolase activity whereas serum from these animals had less effect. Cells and serum from complete Freund's adjuvant-injected control animals also induced structural changes in myelin that were significantly less than changes induced by cells and serum from animals with EAE. These experiments show that lymphoid cells and serum obtained from SJL/J mice with acute EAE affected myelin biochemistry and morphology in syngeneic CNS cultures.
 ...
PMID:Correlation between 2',3'-cyclic nucleotide 3'-phosphohydrolase activity and demyelination in vitro using a syngeneic system. 298 Dec 90

Powassan virus strain M794, a member of the Flavivirus genus known to infect man and animals in Canada, was inoculated intracerebrally into rabbits and horses. No clinical signs were observed in rabbits, but widespread encephalitis resulted, characterized by lymphoid perivascular cuffing, lymphocytic meningitis, and lymphocytic choroiditis. In horses, eight days after inoculation, prominent neurological signs occurred and lesions were those of non-suppurative encephalomyelitis, neuronal necrosis, and focal parenchymal necrosis. The virus could not be reisolated from the rabbit or horse brains. Pathologic features, useful in separating some of the common North American equine neurological diseases, are discussed.
 ...
PMID:Powassan viral encephalitis: a review and experimental studies in the horse and rabbit. 299 3

Japanese encephalitis and postmeasles encephalomyelitis represent two important forms of acute encephalitis in the developing world. Japanese encephalitis accounts for 20,000 acute illnesses per year, and measles encephalomyelitis accounts for as many as 100,000. Both are accompanied by mortalities of 20%-30%, and in both forms, approximately one-half of the survivors have neurological sequelae. Therefore, these two diseases are responsible for a considerable proportion of worldwide mental and motor disabilities. Furthermore, both diseases are preventable with use of safe vaccines. Despite these similarities, their very different pathologies appear to be based on different mechanisms of pathogenesis (table 2). In Japanese encephalitis there is direct invasion of the virus into the nervous system, selective infection and destruction of neurons, and evidence that both humoral and cellular immune responses attenuate the infection. In measles encephalomyelitis there is little evidence that the virus invades the nervous system. Rather, measles virus infects lymphoid cells and causes abnormalities in immune regulation. Humoral immune responses are not found within the nervous system, and the cellular immune response may be inappropriately directed against host antigens. In measles encephalomyelitis, the inflammatory cells entering the nervous system may be the effector cells of autoimmune disease.
 ...
PMID:The pathogenesis of acute viral encephalitis and postinfectious encephalomyelitis. 302 98

Using peroxidase immunohistochemistry and in situ hybridization to localize viral antigen and RNA, we studied autopsy tissues from 20 cases of acute fatal human measles (including seven patients with acute encephalomyelitis) and peripheral blood mononuclear cells from 16 patients with acute, nonfatal measles. In immunologically normal patients, virus was detected in five of nine who died five days or less after the onset of rash but in none of 11 who died later. Virus was localized to epithelial cells of lung, gut, bile duct, bladder, and skin and to lymphoid organs. Neither viral antigen nor RNA was detected in brain sections from 14 patients, including seven with acute encephalomyelitis and four with virus identified in other tissues, a finding supporting an indirect pathogenesis of post-measles encephalomyelitis. These data show that measles virus replicates in cells previously not recognized to be involved (capillary endothelium of lymph node and thymus, Hassall's corpuscles, and hepatic duct epithelium) and that invasion of the brain parenchyma during acute measles is uncommon.
 ...
PMID:Acute measles in patients with and without neurological involvement: distribution of measles virus antigen and RNA. 304 79

Central nervous system (CNS) depletion of norepinephrine (NE) using 6-hydroxydopamine (6-OHDA) prior to disease induction suppressed the clinical signs of experimental autoimmune encephalomyelitis (EAE). This treatment did not have an effect on the degree of mononuclear cell infiltration when spinal cord sections were examined and stained with hematoxylin and eosin, nor on serum levels of anti-myelin basic protein antibodies. However, investigation of the subpopulations of lymphoid cells within the perivascular lesions showed an increase in cells bearing the T suppressor cell phenotype, OX8+, in the 6-OHDA-treated EAE rats when compared to saline-control-treated EAE rats. Examination of other cellular subsets showed no differences in the numbers of T helper cells, macrophages, or B cells within the lesions of the two groups. Furthermore, histofluorescent estimation of catecholamines in spinal cord sections from 6-OHDA- and saline-control-treated EAE rats demonstrated that catecholamines were indeed depleted in the rats with suppressed clinical EAE. These findings suggest that 6-OHDA depletion of CNS NE may remove an effector amplification mechanism, or trigger a T suppressor cell mechanism, or both, leading to suppression of the effector phase of EAE, clinical paralysis.
 ...
PMID:Central catecholamine neurotoxin administration. 1. Immunological changes associated with the suppression of experimental autoimmune encephalomyelitis. 312 18

Rats dying acutely of experimental auto-immune encephalomyelitis show very meagre histological signs of the disease in routine histology sections. This cannot be explained by postmortal changes. It is suggested that the infiltrating lymphoid cells seen in the central nervous system for surviving rats are involved in the normally occurring self-limitation of the disease.
 ...
PMID:Lack of histological signs in rats dying during the acute phase of experimental auto-immune encephalomyelitis. 348 85


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>