Inflammation is a component of neurodegeneration in response to Venezuelan equine encephalitis virus infection in mice
Infection with the mosquito-transmitted Venezuelan equine encephalitis virus (VEE) causes an acute systemic febrile illness followed by meningoencephalitis. In this communication we characterize the cytokine profile induced in the central nervous system (CNS) in response to virulent or attenuated st...
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| Veröffentlicht in: | Journal of neuroimmunology 2000-09, Vol.109 (2), p.132-146 |
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| creator | Schoneboom, Bruce A Catlin, Kristen M.K Marty, Aileen M Grieder, Franziska B |
| description | Infection with the mosquito-transmitted Venezuelan equine encephalitis virus (VEE) causes an acute systemic febrile illness followed by meningoencephalitis. In this communication we characterize the cytokine profile induced in the central nervous system (CNS) in response to virulent or attenuated strains of VEE using RNase Protection Assays. Virulent VEE causes an upregulation of multiple pro-inflammatory genes including inducible nitric oxide synthase (iNOS) and tumor necrosis factor alpha (TNF-α). To determine if iNOS and TNF-α contribute to the neuropathogenesis of VEE infection, iNOS and TNF receptor knockout mice were used in VEE mortality studies and exhibited extended survival times. Finally, CNS tissue sections labeled for VEE antigen, and adjacent sections double-labeled for an astrocyte marker and apoptosis, revealed that apoptosis of neurons occurs not only in areas of the brain positive for VEE-antigen, but also in areas of astrogliosis. These findings suggest that the inflammatory response, which is in part mediated by iNOS and TNF-α, may contribute to neurodegeneration following encephalitic virus infection. |
| doi_str_mv | 10.1016/S0165-5728(00)00290-3 |
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In this communication we characterize the cytokine profile induced in the central nervous system (CNS) in response to virulent or attenuated strains of VEE using RNase Protection Assays. Virulent VEE causes an upregulation of multiple pro-inflammatory genes including inducible nitric oxide synthase (iNOS) and tumor necrosis factor alpha (TNF-α). To determine if iNOS and TNF-α contribute to the neuropathogenesis of VEE infection, iNOS and TNF receptor knockout mice were used in VEE mortality studies and exhibited extended survival times. Finally, CNS tissue sections labeled for VEE antigen, and adjacent sections double-labeled for an astrocyte marker and apoptosis, revealed that apoptosis of neurons occurs not only in areas of the brain positive for VEE-antigen, but also in areas of astrogliosis. 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In this communication we characterize the cytokine profile induced in the central nervous system (CNS) in response to virulent or attenuated strains of VEE using RNase Protection Assays. Virulent VEE causes an upregulation of multiple pro-inflammatory genes including inducible nitric oxide synthase (iNOS) and tumor necrosis factor alpha (TNF-α). To determine if iNOS and TNF-α contribute to the neuropathogenesis of VEE infection, iNOS and TNF receptor knockout mice were used in VEE mortality studies and exhibited extended survival times. Finally, CNS tissue sections labeled for VEE antigen, and adjacent sections double-labeled for an astrocyte marker and apoptosis, revealed that apoptosis of neurons occurs not only in areas of the brain positive for VEE-antigen, but also in areas of astrogliosis. These findings suggest that the inflammatory response, which is in part mediated by iNOS and TNF-α, may contribute to neurodegeneration following encephalitic virus infection.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - immunology</subject><subject>Astrocytes - cytology</subject><subject>Astrocytes - immunology</subject><subject>Astrocytes - virology</subject><subject>Brain Edema - immunology</subject><subject>Brain Edema - virology</subject><subject>Cells, Cultured</subject><subject>Cytokines</subject><subject>Encephalitis Virus, Venezuelan Equine</subject><subject>Encephalomyelitis, Venezuelan Equine - immunology</subject><subject>Encephalomyelitis, Venezuelan Equine - mortality</subject><subject>Female</subject><subject>Gene Expression Regulation, Viral - immunology</subject><subject>Gliosis - immunology</subject><subject>Gliosis - virology</subject><subject>In Situ Nick-End Labeling</subject><subject>Inflammation</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Nerve Degeneration - immunology</subject><subject>Nerve Degeneration - virology</subject><subject>Neurodegeneration</subject><subject>Neuroimmunomodulation - immunology</subject><subject>Neurons - cytology</subject><subject>Neurons - immunology</subject><subject>Neurons - virology</subject><subject>neurovirology</subject><subject>Nitric Oxide Synthase - genetics</subject><subject>Nitric Oxide Synthase - immunology</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Phenotype</subject><subject>Survival Analysis</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - immunology</subject><subject>Venezuelan equine encephalitis virus</subject><subject>Venezuelan equine encephalitis virus (VEE)</subject><issn>0165-5728</issn><issn>1872-8421</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUFv1DAQhS0EotvCTwD5hMohMI7jOD4hVJVSqVIPBa6W7YzBKLG3drIS_Hq83QVx62XmMN-bGb1HyCsG7xiw_v1dLaIRsh3OAd4CtAoa_oRs2CDbZuha9pRs_iEn5LSUnwBM8E49JycMlOpbJjZkdx39ZObZLCFFGgo11KV5myLGhSZPI645jfgdI-YjE2nGUomCdEn0W538XnEykeL9GiJSjA63P8wUlrpuF_Jaqsaj-6ueg8MX5Jk3U8GXx35Gvn66_HLxubm5vbq--HjTOK7apbGj8RKd5cgHg0oqb5nwPePWCtH5EVwnEUblLHOd4JbBgKzno3VKAEPLz8ibw95tTvcrlkXPoTic6ruY1qJl2w7twOSjIJO9lNDxCooD6HIqJaPX2xxmk39pBnqfjH5IRu9t1wD6IRm9170-HljtjON_qkMUFfhwALD6sQuYdXFh7-UYcjVPjyk8cuIPo7mg0w</recordid><startdate>20000922</startdate><enddate>20000922</enddate><creator>Schoneboom, Bruce A</creator><creator>Catlin, Kristen M.K</creator><creator>Marty, Aileen M</creator><creator>Grieder, Franziska B</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TK</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20000922</creationdate><title>Inflammation is a component of neurodegeneration in response to Venezuelan equine encephalitis virus infection in mice</title><author>Schoneboom, Bruce A ; Catlin, Kristen M.K ; Marty, Aileen M ; Grieder, Franziska B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c392t-bdaf7ecb3e38ae979fb15f613bb554fd0c47e0d9cb1c453b108e163dbc9501eb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - immunology</topic><topic>Astrocytes - cytology</topic><topic>Astrocytes - immunology</topic><topic>Astrocytes - virology</topic><topic>Brain Edema - immunology</topic><topic>Brain Edema - virology</topic><topic>Cells, Cultured</topic><topic>Cytokines</topic><topic>Encephalitis Virus, Venezuelan Equine</topic><topic>Encephalomyelitis, Venezuelan Equine - immunology</topic><topic>Encephalomyelitis, Venezuelan Equine - mortality</topic><topic>Female</topic><topic>Gene Expression Regulation, Viral - immunology</topic><topic>Gliosis - immunology</topic><topic>Gliosis - virology</topic><topic>In Situ Nick-End Labeling</topic><topic>Inflammation</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Nerve Degeneration - immunology</topic><topic>Nerve Degeneration - virology</topic><topic>Neurodegeneration</topic><topic>Neuroimmunomodulation - immunology</topic><topic>Neurons - cytology</topic><topic>Neurons - immunology</topic><topic>Neurons - virology</topic><topic>neurovirology</topic><topic>Nitric Oxide Synthase - genetics</topic><topic>Nitric Oxide Synthase - immunology</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Phenotype</topic><topic>Survival Analysis</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - immunology</topic><topic>Venezuelan equine encephalitis virus</topic><topic>Venezuelan equine encephalitis virus (VEE)</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schoneboom, Bruce A</creatorcontrib><creatorcontrib>Catlin, Kristen M.K</creatorcontrib><creatorcontrib>Marty, Aileen M</creatorcontrib><creatorcontrib>Grieder, Franziska B</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neuroimmunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schoneboom, Bruce A</au><au>Catlin, Kristen M.K</au><au>Marty, Aileen M</au><au>Grieder, Franziska B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inflammation is a component of neurodegeneration in response to Venezuelan equine encephalitis virus infection in mice</atitle><jtitle>Journal of neuroimmunology</jtitle><addtitle>J Neuroimmunol</addtitle><date>2000-09-22</date><risdate>2000</risdate><volume>109</volume><issue>2</issue><spage>132</spage><epage>146</epage><pages>132-146</pages><issn>0165-5728</issn><eissn>1872-8421</eissn><abstract>Infection with the mosquito-transmitted Venezuelan equine encephalitis virus (VEE) causes an acute systemic febrile illness followed by meningoencephalitis. In this communication we characterize the cytokine profile induced in the central nervous system (CNS) in response to virulent or attenuated strains of VEE using RNase Protection Assays. Virulent VEE causes an upregulation of multiple pro-inflammatory genes including inducible nitric oxide synthase (iNOS) and tumor necrosis factor alpha (TNF-α). To determine if iNOS and TNF-α contribute to the neuropathogenesis of VEE infection, iNOS and TNF receptor knockout mice were used in VEE mortality studies and exhibited extended survival times. Finally, CNS tissue sections labeled for VEE antigen, and adjacent sections double-labeled for an astrocyte marker and apoptosis, revealed that apoptosis of neurons occurs not only in areas of the brain positive for VEE-antigen, but also in areas of astrogliosis. 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| subjects | Animals Apoptosis Apoptosis - immunology Astrocytes - cytology Astrocytes - immunology Astrocytes - virology Brain Edema - immunology Brain Edema - virology Cells, Cultured Cytokines Encephalitis Virus, Venezuelan Equine Encephalomyelitis, Venezuelan Equine - immunology Encephalomyelitis, Venezuelan Equine - mortality Female Gene Expression Regulation, Viral - immunology Gliosis - immunology Gliosis - virology In Situ Nick-End Labeling Inflammation Mice Mice, Inbred C57BL Mice, Knockout Nerve Degeneration - immunology Nerve Degeneration - virology Neurodegeneration Neuroimmunomodulation - immunology Neurons - cytology Neurons - immunology Neurons - virology neurovirology Nitric Oxide Synthase - genetics Nitric Oxide Synthase - immunology Nitric Oxide Synthase Type II Phenotype Survival Analysis Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - immunology Venezuelan equine encephalitis virus Venezuelan equine encephalitis virus (VEE) |
| title | Inflammation is a component of neurodegeneration in response to Venezuelan equine encephalitis virus infection in mice |
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