Relevant bibliographies by topics / Experimental Autoimmune Neuritis

Academic literature on the topic 'Experimental Autoimmune Neuritis'

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Published: 4 June 2021
Last updated: 21 February 2023

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Journal articles on the topic "Experimental Autoimmune Neuritis"

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Fujioka, Toshiki. "Experimental autoimmune neuritis." Clinical and Experimental Neuroimmunology 9, no. 2 (May 2018): 84–92. http://dx.doi.org/10.1111/cen3.12461.

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Kezuka, Takeshi, Yoshihiko Usui, and Hiroshi Goto. "Analysis of the Pathogenesis of Experimental Autoimmune Optic Neuritis." Journal of Biomedicine and Biotechnology 2011 (2011): 1–5. http://dx.doi.org/10.1155/2011/294046.

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Optic neuritis associated with multiple sclerosis has a strong association with organ-specific autoimmune disease. The goal of our research is to establish an optimal organ-specific animal model to elucidate the pathogenetic mechanisms of the disease and to develop therapeutic strategies using the model. This paper is divided into five sections: (1) clinical picture of optic neuritis associated with multiple sclerosis, (2) elucidation of pathogenesis using animal models with inflammation in optic nerve and spinal cord, (3) clinical relevance of concurrent encephalomyelitis in optic neuritis model, (4) retinal damage in a concurrent multiple sclerosis and optic neuritis model, and (5) development of novel therapies using mouse optic neuritis model. Advanced therapies using biologicals have succeeded to control intractable optic neuritis in animal models. This may ultimately lead to prevention of vision loss within a short period from acute onset of optic neuritis in human. By conducting research flexibly, ready to switch from the bench to the bedside and from the bedside to the bench as the opportunity arises, this strategy may help to guide the research of optic neuritis in the right direction.
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Zhang, Cun‐Jin, Hui Zhai, Yaping Yan, Junwei Hao, Min‐Shu Li, Wei‐Na Jin, Ning Su, Timothy L. Vollmer, and Fu‐Dong Shi. "Glatiramer acetate ameliorates experimental autoimmune neuritis." Immunology & Cell Biology 92, no. 2 (November 26, 2013): 164–69. http://dx.doi.org/10.1038/icb.2013.81.

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Calik, Michael W., Sahadev A. Shankarappa, and Evan B. Stubbs. "Forced-exercise attenuates experimental autoimmune neuritis." Neurochemistry International 61, no. 2 (July 2012): 141–45. http://dx.doi.org/10.1016/j.neuint.2012.04.023.

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Wang, N., J. Chapman, R. Rabinowitz, S. Viskin, M. Kafri, and A. D. Korczyn. "Autonomic dysfunction in experimental autoimmune neuritis:." Journal of the Neurological Sciences 184, no. 2 (March 2001): 183–88. http://dx.doi.org/10.1016/s0022-510x(01)00444-0.

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Han, Fuyu, Bangwei Luo, Rongchen Shi, Changhao Han, Zhonghao Zhang, Jian Xiong, Man Jiang, and Zhiren Zhang. "Curcumin ameliorates rat experimental autoimmune neuritis." Journal of Neuroscience Research 92, no. 6 (January 31, 2014): 743–50. http://dx.doi.org/10.1002/jnr.23357.

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Shin, Taekyun, Meejung Ahn, Changjong Moon, and Seungjoon Kim. "Erythropoietin and autoimmune neuroinflammation: lessons from experimental autoimmune encephalomyelitis and experimental autoimmune neuritis." Anatomy & Cell Biology 45, no. 4 (2012): 215. http://dx.doi.org/10.5115/acb.2012.45.4.215.

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Gabriel, C. "Human immunoglobulin ameliorates rat experimental autoimmune neuritis." Brain 120, no. 9 (September 1, 1997): 1533–40. http://dx.doi.org/10.1093/brain/120.9.1533.

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Hughes, P. "Matrix metalloproteinase expression during experimental autoimmune neuritis." Brain 121, no. 3 (March 1, 1998): 481–94. http://dx.doi.org/10.1093/brain/121.3.481.

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Korn, T. "Suppression of experimental autoimmune neuritis by leflunomide." Brain 124, no. 9 (September 1, 2001): 1791–802. http://dx.doi.org/10.1093/brain/124.9.1791.

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Dissertations / Theses on the topic "Experimental Autoimmune Neuritis"

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Zou, Li-Ping. "Immunoregulation and immunotherapy in experimental autoimmune neuritis /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3918-7/.

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Bao, Lei. "Immunomodulation and immunopathogenesis in the autoimmune disease with emphasis on autoimmune neuritis and arthritis /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-447-X/.

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Zhu, Yu. "Immunoregulation of experimental autoimmune neuritis focuses on cell immunity /." Stockholm, 2003. http://diss.kib.ki.se/2003/isbn/.

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Duan, Rui-Sheng. "Inflammation and neurodegeneration in mouse nervous system: experimental application /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-606-9/.

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Lin, Hsin Hsin. "Mechanisms of Intravenous Immunoglobulin in the Treatment of Experimental Autoimmune Neuritis." University of Sydney, 2007. http://hdl.handle.net/2123/1696.

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PhD
The aims of this study were to test the efficacy of immunoglobulin and its Fab and Fc fragment in the treatment of experimental autoimmune neuritis (EAN) in Lewis rats, to investigate which portion of immunoglobulin is operative in the effect of IVIg, and to clarify the possible mechanisms by which immunoglobulin exerts its action in the treatment of rats EAN. EAN was induced by immunization with whole bovine peripheral nerve myelin. The immunized rats were randomized into groups, assessed clinically, electrophysiologically, and histologically, and intravenously injected with normal saline, albumin, human IVIg preparation, purified Fab or Fc fragments. The treatment efficacy was compared between normal saline and albumin groups, albumin and IVIg groups, albumin and Fab groups, albumin and Fc groups, Fab and Fc groups, Fab and IVIg groups, and Fc and IVIg groups. Methods of myelin isolation, antibody purification, and Western blot techniques were also applied. The results revealed that treatment with Fc fragment and IVIg at the onset of signs of disease effectively prevented further progression of disease, shortened disease duration, and facilitating recovery from illness as shown in clinical, electrophysiological and histological parameters. In the study which the efficacy of albumin and IVIg was compared, 5 out of 17 rats (29%) in the albumin group and 12 out of 17 (71%) in the IVIg group completely recovered from the clinical disease by day 30. The animals receiving IVIg treatment exhibited lower clinical scores, less prolongation of S wave latencies, better maintained S wave amplitudes, less reduction of distal motor NCVs, better maintained distal and proximal CMAP amplitudes, and lower histological grades. In the study which the efficacy of albumin, Fab fragment, Fc fragment, and IVIg was compared, 0 out of 8 (0%) in the albumin group, 1 out of 8 (13%) in the Fab group, 4 out of 8 (50%) in the Fc group, and 6 out of 9 (67%) rats in the IgG group completely recovered from the clinical disease by day 30. The animals receiving Fc fragment and IVIg treatment exhibited lower clinical scores, less prominent weight loss, less prolongation of S wave latencies, better maintained S wave amplitudes, less reduction of distal motor NCVs, better maintained distal and proximal CMAP amplitudes, and lower histological grades.
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Lin, Hsin Hsin. "Mechanisms of Intravenous Immunoglobulin in the Treatment of Experimental Autoimmune Neuritis." Thesis, The University of Sydney, 2006. http://hdl.handle.net/2123/1696.

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The aims of this study were to test the efficacy of immunoglobulin and its Fab and Fc fragment in the treatment of experimental autoimmune neuritis (EAN) in Lewis rats, to investigate which portion of immunoglobulin is operative in the effect of IVIg, and to clarify the possible mechanisms by which immunoglobulin exerts its action in the treatment of rats EAN. EAN was induced by immunization with whole bovine peripheral nerve myelin. The immunized rats were randomized into groups, assessed clinically, electrophysiologically, and histologically, and intravenously injected with normal saline, albumin, human IVIg preparation, purified Fab or Fc fragments. The treatment efficacy was compared between normal saline and albumin groups, albumin and IVIg groups, albumin and Fab groups, albumin and Fc groups, Fab and Fc groups, Fab and IVIg groups, and Fc and IVIg groups. Methods of myelin isolation, antibody purification, and Western blot techniques were also applied. The results revealed that treatment with Fc fragment and IVIg at the onset of signs of disease effectively prevented further progression of disease, shortened disease duration, and facilitating recovery from illness as shown in clinical, electrophysiological and histological parameters. In the study which the efficacy of albumin and IVIg was compared, 5 out of 17 rats (29%) in the albumin group and 12 out of 17 (71%) in the IVIg group completely recovered from the clinical disease by day 30. The animals receiving IVIg treatment exhibited lower clinical scores, less prolongation of S wave latencies, better maintained S wave amplitudes, less reduction of distal motor NCVs, better maintained distal and proximal CMAP amplitudes, and lower histological grades. In the study which the efficacy of albumin, Fab fragment, Fc fragment, and IVIg was compared, 0 out of 8 (0%) in the albumin group, 1 out of 8 (13%) in the Fab group, 4 out of 8 (50%) in the Fc group, and 6 out of 9 (67%) rats in the IgG group completely recovered from the clinical disease by day 30. The animals receiving Fc fragment and IVIg treatment exhibited lower clinical scores, less prominent weight loss, less prolongation of S wave latencies, better maintained S wave amplitudes, less reduction of distal motor NCVs, better maintained distal and proximal CMAP amplitudes, and lower histological grades.
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Dahlman, Ingrid. "Genetic dissection of experimental autoimmune neuroinflammatory diseases in rats /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3768-0/.

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Mendes, Vania Alice de Aguiar. "Indução da neurite autoimune experimental (NAE) em camundongos SJL/J através de injeção de proteína P2 da mielina do nervo periférico (MNP)." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/17/17140/tde-12012017-143733/.

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A neurite auto-imune experimental (NAE) é uma polineuropatia desmielinizante monofásica do sistema nervoso periférico (SNP). A NAE é considerada modelo experimental da síndrome de Guillain-Barré (SGB). Por se tratar de uma doença autoimune, pode ser induzida experimentalmente em camundongos geneticamente susceptíveis, através da imunização com componentes da mielina de nervos periféricos. Para a indução da NAE podem ser utilizados P0 e P2, proteínas da mielina do nervo periférico, ou sequências conhecidas de peptídeos dessas proteínas 180-199 e 58-81 respectivamente, consideradas neuritogênicas, ou ainda transferência adotiva de lifócitos T CD4+, oriundas de camundongos previamente imunizados. Para o presente estudo foram utilizados camundongos fêmeas SJL/J nãográvidas, com idade entre 8 e 12 semanas, pesando de 17 a 20 g. Os animais foram divididos em dois grupos: um controle e outro com NAE. 200 µg da sequência de peptídeos 58-81 de P2 emulsificada em 100 µl de adjuvante de Freund completo (AFC) foram injetados por via subcutânea, em quatro locais na região lombar. Para os controles, foi utilizado solução tamponada de fosfato (PBS), emulsionada em AFC desprovida da sequência 58-81 de peptídeos P2, injetada no mesmo local, na mesma quantidade e forma. Cada camundongo tratado com P2 recebeu 200 ng de toxina pertussis em 100 ?L de PBS intraperitonealmente (i.p.) nos dias 0 e 2 pós-imunização (p.i.). No grupo controle, volumes iguais de PBS e toxina pertussis foram administrados pela mesma via sem o peptídeo. Avaliações da motricidade foram realizadas diariamente até o 60º dia, além de análises funcionais e eletroneuromiográficas. Foram encontradas alterações exclusivamente eletrofisiológicas, desmielinizantes e axonais, em cerca de dois terços dos camundongos. Sendo o camundongo SJL/J considerado o camundongo mais susceptível para a provocação de NAE, os achados do presente estudo indicam a limitação do modelo: ausência de alterações motoras detectáveis clinicamente, ocorrendo distúrbios eletrofisiológicos em apenas parte dos animais. O melhor modelo de NAE continua sendo o provocado no rato Lewis por proteína da mielina periférica bovina. É desejável que se continue buscando modelo experimental de NAE em camundongos, tendo em vista que essa espécie animal é a mais bem estudada na Biologia animal e, por essa razão, dela haver extensa variedade de imunobiológicos disponíveis para estudo da patogenia e fisiopatologia de doenças auto-imunes.
Experimental autoimmune neurits (EAN) is a monophasic demyelinating disease of the peripheral nervous system (PNS). EAN is considered to be the experimental model for Guillain-Barré syndrome (GBS). EAN can be induced in genetically susceptible mice using peripheral myelin components as immunogens: peripheral nerve myelin proteins P0 or P2; peptides sequences of those proteins considered neuritogenic, or the adoptive transfer of TCD4+ lymphocytes from previously immunized mice. In the present study non-pregnant female SJL/J mice aged 8-12 weeks weighint 17-20 g where used. The experimental group was treated as follows. Peptides sequence of P2 (200 µg) emulsified in complete Freund adjuvant (CFA) (100 µl) injected in four sites at the lumbar paravertebral region s.c. Controls were injected in the same sites with equal quantities of phosphate buffer solution emulsified in CFA without the peptides sequence. Each mouse treated with P2 was also treated with 200 ng pertussis toxin in 100 ?L PBS i.p. at the days 0 and 2 post-immunisation. Controls were injected i.p. with equal volumes of PBS and pertussis toxin free of the peptides sequence. Motor strength, posture and coordination were evaluated daily until the 60th day postinoculation besides eletroneuromyographic (EMG) evaluation on the 10th and 30thy days of some mice. No clinical disturbances were observed and in two thirds of the animals demyelinating and axonal features were detected at the EMG. SJL/J mice are considered the most susceptible mouse strain for NAE induction but the findings of the present study indicates the limitations of the model and its reproducibility. The best NAE model is yet the obtained in Lewis rat. It is important to look for a mouse model of EAN because this animal species is the most studied in the animal Biology. The extensive variety of immunobiologic products from mice allows performing studies on the pathogeny or physiopathology of autoimmune diseases more easily.
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Castro, Fabiano Roberto de. "Efeito da crotapotina na evolução clinica da neurite experimental autoimune (EAN)." [s.n.], 2006. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310330.

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Orientador: Leonilda Maria Barbosa dos Santos
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A Síndrome de Guillain-Barré (SGB) é uma doença desmielinizante do sistema nervoso periférico (SNP). Baseado principalmente nas similaridades clínicas e histopatológicas a Neurite Experimental Auto-imune (EAN) tem sido extensivamente usada como modelo de estudo da SGB. A EAN é uma doença auto-imune, que pode ser experimentalmente induzida em ratos geneticamente suscetíveis através da imunização com os componentes da mielina de nervos periféricos tais como os peptídeos P0 e P2 , ou ainda por transferência adotiva de lifócitos T CD4+ do tipo Th1. Diferentes tentativas de tratamentos para a SGB têm sido estudadas, dentre elas pode-se citar a plasmaferese, o uso de anticorpos monoclonais, administração de corticóides e a imunossupressão global através da administração de intérferon ß. A utilização de venenos totais de serpentes, ou frações deles, já demonstrou bons resultados na tentativa de tratamento de alguns modelos de doenças auto-imunes como a diabetes auto-imune insulino dependente, lúpus e encefalomielite experimental auto-imune (EAE). No presente trabalho foi estudado o efeito de uma fração do veneno da cascavel sul americana Crotalus durissus terrificus (Cdt), a crotapotina, no modelo de EAN. São apresentadas evidências de que tanto a administração intraperitoneal (IP) como a oral de crotapotina reduz significativamente a gravidade da EAN induzida em ratos Lewis, associada a um significativo declínio na resposta proliferativa das células T neuritogênicas, assim como diminuição de infiltrados de células mononucleares no nervo ciático dos os animais
Abstract: Biomedical research in which venom components are being investigated for their potential as novel therapeutic agents has emerged as an interesting option. Crotapotin which is a fraction of the venom of the rattlesnake Crotalus durissus terrificus, has been described as an antinflammatory that acts on the innate arm of the immune response. Here we have demonstrated that intraperitoneal (IP), as well as oral administration of crotapotin significantly reduces the severity of experimental autoimmune neuritis (EAN), an experimental model for Guillain-Barré Syndrome. The reduction of the severity of the disease is associated with a reduction in the mononuclear cells infiltrating in the sciatic nerve and a significant decrease in the lymphocyte proliferative response to neuritogenic peptide
Mestrado
Ciencias Basicas
Mestre em Clinica Medica
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Soares, Rubens Murilo Gibaile. "Avaliação da cinética da neurite óptica em modelo animal de encefalomielite autoimune experimental induzido por duas diferentes concentrações de glicoproteína dos oligodendrócitos da mielina." Universidade Federal de Juiz de Fora, 2013. https://repositorio.ufjf.br/jspui/handle/ufjf/1410.

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CAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
CNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológico
FAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Gerais
O modelo de Encefalomielite Autoimune Experimental (EAE) é o mais utilizado no estudo da neurite óptica. Este trabalho tem como objetivo avaliar a cinética da neurite óptica em modelo animal de EAE induzido por duas diferentes concentrações de Glicoproteína dos Oligodendrócitos da Mielina (MOG). Para a indução da EAE foram utilizadas fêmeas de camundongos da linhagem C57BL/6, divididas em dois grupos, um grupo induzido com 100 μg de MOG35-55 e um segundo grupo induzido com 300 μg de MOG35-55. Os animais foram diariamente avaliados por meio da análise do escore clínico entre os dias zero e 58 pós-imunização. Nos dias 7, 10, 14, 21 ou 58 pósimunização, os animais foram submetidos a eutanásia, e os nervos ópticos, dissecados em seu trajeto desde a parte posterior do globo ocular até o quiasma óptico. Posteriormente, foram avaliados os aspectos morfológico e imuno-histoquímico dos nervos ópticos. As alterações histopatológicas observadas em um ou em ambos os nervos ópticos consistiram de infiltrado celular inflamatório, tendo a neurite óptica gravidade diferente nos dois grupos estudados. A quimiocina CCL5 foi avaliada no dia 10 pós-imunização, primeiro dia em que foi detectado o infiltrado inflamatório. Os resultados sugerem que duas diferentes concentrações de MOG35-55 utilizadas na indução do modelo animal de EAE induzem duas diferentes formas de evolução da neurite óptica.
The model of Experimental Autoimmune Encephalomyelitis (EAE) is the most used model in the study of optic neuritis. This study aims to evaluate the kinetics of optic neuritis in the EAE animal model induced by two different concentrations of Oligodendrocytes Myelin Glycoprotein (MOG). For induction of EAE were used female mice of the C57BL/6 lineage, divided into two groups, one group induced with 100 μg of MOG35-55 and a second group induced with 300 μg of MOG35-55. The animals were evaluated daily by analysis of clinical score between zero and 58 days after immunization. On days 7, 10, 14, 21 or 58 post-immunization, the animals were euthanized. The optic nerves were dissected from the back of the eyeball to the optic chiasm; subsequently the morphological and immunohistochemical aspects of the optic nerves were evaluated. The histopathological changes observed in one or in both optic nerves consisted of inflammatory cell infiltrate. Optic neuritis had different levels of severity in the two groups. The chemokine CCL5 was evaluated on day 10 post-immunization, the first day when the inflammatory infiltrate was detected. The results suggest that two different concentrations of MOG35-55 used in the induction of EAE animal model induce two different forms of optic neuritis evolution.
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Book chapters on the topic "Experimental Autoimmune Neuritis"

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Guyton, M. K., A. W. Smith, S. K. Ray, and N. L. Banik. "Experimental Autoimmune Encephalomyelitis in the Pathogenesis of Optic Neuritis: Is Calpain Involved?" In Handbook of Neurochemistry and Molecular Neurobiology, 525–41. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-30375-8_22.

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Gonsalvez, David G., SangWon Yoo, Georgina A. Craig, Rhiannon J. Wood, Jessica L. Fletcher, Simon S. Murray, and Junhua Xiao. "Myelin Protein Zero180–199 Peptide Induced Experimental Autoimmune Neuritis in C57BL/6 Mice." In Methods in Molecular Biology, 243–50. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7862-5_19.

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Linington, Christopher, and Hartmut Wekerle. "Experimental Autoimmune Neuritis." In Autoimmune Disease Models, 39–56. Elsevier, 1994. http://dx.doi.org/10.1016/b978-0-08-091736-8.50008-8.

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"Experimental autoimmune neuritis." In Autoimmune Neurological Disease, 177–201. Cambridge University Press, 1995. http://dx.doi.org/10.1017/cbo9780511526916.008.

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GOLD, RALF, GUIDO STOLL, BERND C. KIESEIER, HANS-PETER HARTUNG, and KLAUS V. TOYKA. "Experimental Autoimmune Neuritis." In Peripheral Neuropathy, 609–33. Elsevier, 2005. http://dx.doi.org/10.1016/b978-0-7216-9491-7.50030-2.

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Narayanan, S. Priya, Abdelrahman Y. Fouda, Fang Liu, and Shengshuai Shan. "The mouse model of experimental autoimmune encephalomyelitis: Methods to study neuroinflammation in optic neuritis." In Handbook of Animal Models in Neurological Disorders, 391–402. Elsevier, 2023. http://dx.doi.org/10.1016/b978-0-323-89833-1.00011-2.

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