Immunology and Oxidative Stress in Multiple Sclerosis: Clinical and Basic Approach
Multiple sclerosis (MS) exhibits many of the hallmarks of an inflammatory autoimmune disorder including breakdown of the blood-brain barrier (BBB), the recruitment of lymphocytes, microglia, and macrophages to lesion sites, the presence of multiple lesions, generally being more pronounced in the bra...
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | Clinical and Developmental Immunology |
| Online Access: | http://dx.doi.org/10.1155/2013/708659 |
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| author | Genaro G. Ortiz Fermín P. Pacheco-Moisés Oscar K. Bitzer-Quintero Ana C. Ramírez-Anguiano Luis J. Flores-Alvarado Viridiana Ramírez-Ramírez Miguel A. Macias-Islas Erandis D. Torres-Sánchez |
| author_facet | Genaro G. Ortiz Fermín P. Pacheco-Moisés Oscar K. Bitzer-Quintero Ana C. Ramírez-Anguiano Luis J. Flores-Alvarado Viridiana Ramírez-Ramírez Miguel A. Macias-Islas Erandis D. Torres-Sánchez |
| author_sort | Genaro G. Ortiz |
| collection | DOAJ |
| description | Multiple sclerosis (MS) exhibits many of the hallmarks of an inflammatory autoimmune disorder including breakdown of the
blood-brain barrier (BBB), the recruitment of lymphocytes, microglia, and macrophages to lesion sites, the presence of multiple lesions, generally
being more pronounced in the brain stem and spinal cord, the predominantly perivascular location of lesions, the temporal maturation of lesions from
inflammation through demyelination, to gliosis and partial remyelination, and the presence of immunoglobulin in the central nervous system and cerebrospinal fluid. Lymphocytes activated in the periphery infiltrate the central nervous system to trigger a local immune response that ultimately damages myelin and axons. Pro-inflammatory cytokines amplify the inflammatory cascade by compromising the BBB, recruiting immune cells from the periphery,
and activating resident microglia. inflammation-associated oxidative burst in activated microglia and macrophages plays an important role in the demyelination and free radical-mediated
tissue injury in the pathogenesis of MS. The inflammatory environment in demyelinating lesions leads to the generation of oxygen- and nitrogen-free radicals as well as proinflammatory cytokines which contribute to the development and progression of the disease. Inflammation can lead to oxidative stress and vice versa. Thus, oxidative stress and inflammation are involved in a self-perpetuating cycle. |
| format | Article |
| id | doaj-art-aa41428d63a84f319f8adebf44b1acf5 |
| institution | Kabale University |
| issn | 1740-2522 1740-2530 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Clinical and Developmental Immunology |
| spelling | doaj-art-aa41428d63a84f319f8adebf44b1acf52025-02-03T01:10:44ZengWileyClinical and Developmental Immunology1740-25221740-25302013-01-01201310.1155/2013/708659708659Immunology and Oxidative Stress in Multiple Sclerosis: Clinical and Basic ApproachGenaro G. Ortiz0Fermín P. Pacheco-Moisés1Oscar K. Bitzer-Quintero2Ana C. Ramírez-Anguiano3Luis J. Flores-Alvarado4Viridiana Ramírez-Ramírez5Miguel A. Macias-Islas6Erandis D. Torres-Sánchez7Laboratorio de Mitocondria-Estrés Oxidativo y Patología, División de Neurociencias, Centro de Investigación Biomédica de Occidente del Instituto Mexicano del Seguro Social, Sierra Mojada 800, CP 44340 Guadalajara, Jalisco, MexicoDepartamento de Química, Centro Universitario de Ciencias de Ciencias Exactas e Ingenierías, Universidad de Guadalajara, Blvd. Marcelino García Barragán 1421 CP 44430 Guadalajara, Jalisco, MexicoLaboratorio de Neuroinmunomodulación, División de Neurociencias, Centro de Investigación Biomédica de Occidente del Instituto Mexicano del Seguro Social, Sierra Mojada 800, CP 44340 Guadalajara, Jalisco, MexicoDepartamento de Química, Centro Universitario de Ciencias de Ciencias Exactas e Ingenierías, Universidad de Guadalajara, Blvd. Marcelino García Barragán 1421 CP 44430 Guadalajara, Jalisco, MexicoDepartamento de Bioquímica, Centro Universitario de Ciencias de Ciencias Exactas de la Salud, Universidad de Guadalajara, Sierra Mojada 950 CP 44350 Guadalajara, Jalisco, MexicoLaboratorio de Mitocondria-Estrés Oxidativo y Patología, División de Neurociencias, Centro de Investigación Biomédica de Occidente del Instituto Mexicano del Seguro Social, Sierra Mojada 800, CP 44340 Guadalajara, Jalisco, MexicoDepartamento de Neurología, Unidad Médica de Alta Especialidad, Centro Médico Nacional de Occidente del Instituto Mexicano del Seguro Social, Belisario Dominguez 1000 CP 44340 Guadalajara, Jalisco, MexicoLaboratorio de Mitocondria-Estrés Oxidativo y Patología, División de Neurociencias, Centro de Investigación Biomédica de Occidente del Instituto Mexicano del Seguro Social, Sierra Mojada 800, CP 44340 Guadalajara, Jalisco, MexicoMultiple sclerosis (MS) exhibits many of the hallmarks of an inflammatory autoimmune disorder including breakdown of the blood-brain barrier (BBB), the recruitment of lymphocytes, microglia, and macrophages to lesion sites, the presence of multiple lesions, generally being more pronounced in the brain stem and spinal cord, the predominantly perivascular location of lesions, the temporal maturation of lesions from inflammation through demyelination, to gliosis and partial remyelination, and the presence of immunoglobulin in the central nervous system and cerebrospinal fluid. Lymphocytes activated in the periphery infiltrate the central nervous system to trigger a local immune response that ultimately damages myelin and axons. Pro-inflammatory cytokines amplify the inflammatory cascade by compromising the BBB, recruiting immune cells from the periphery, and activating resident microglia. inflammation-associated oxidative burst in activated microglia and macrophages plays an important role in the demyelination and free radical-mediated tissue injury in the pathogenesis of MS. The inflammatory environment in demyelinating lesions leads to the generation of oxygen- and nitrogen-free radicals as well as proinflammatory cytokines which contribute to the development and progression of the disease. Inflammation can lead to oxidative stress and vice versa. Thus, oxidative stress and inflammation are involved in a self-perpetuating cycle.http://dx.doi.org/10.1155/2013/708659 |
| spellingShingle | Genaro G. Ortiz Fermín P. Pacheco-Moisés Oscar K. Bitzer-Quintero Ana C. Ramírez-Anguiano Luis J. Flores-Alvarado Viridiana Ramírez-Ramírez Miguel A. Macias-Islas Erandis D. Torres-Sánchez Immunology and Oxidative Stress in Multiple Sclerosis: Clinical and Basic Approach Clinical and Developmental Immunology |
| title | Immunology and Oxidative Stress in Multiple Sclerosis: Clinical and Basic Approach |
| title_full | Immunology and Oxidative Stress in Multiple Sclerosis: Clinical and Basic Approach |
| title_fullStr | Immunology and Oxidative Stress in Multiple Sclerosis: Clinical and Basic Approach |
| title_full_unstemmed | Immunology and Oxidative Stress in Multiple Sclerosis: Clinical and Basic Approach |
| title_short | Immunology and Oxidative Stress in Multiple Sclerosis: Clinical and Basic Approach |
| title_sort | immunology and oxidative stress in multiple sclerosis clinical and basic approach |
| url | http://dx.doi.org/10.1155/2013/708659 |
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