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The Impact of Social Stress on Central Nervous System Inflammation and T Cell Response to Theiler?s Virus Infection

机译:社会压力对泰勒病毒感染中枢神经系统炎症和T细胞反应的影响

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摘要

Agrowingbodyofevidencesuggeststhatsocialstresscontributestothepathogenesisofneurodegenerativediseases,suchasmultiplesclerosis(MS).Forexample,priorresearchhasshownthatsocialdisruption(SDR)stressbehaviorallyandimmunologicallyexacerbatesTheiler?smurineencephalomyelitisvirus(TMEV)infection.TMEVinfectionresultsinacuteinfectionofthecentralnervoussystem(CNS)followedbyachronicdemyelinatingautoimmunedisease,similartothatseeninMS.Researchsuggeststhatsocialstressexertstheseeffectsbyalteringtheimmuneresponsetoinfection.Morespecifically,itishypothesizedthatSDRsensitizestheacuteinflammatoryresponsetoinfectionandsuppressesTcelleffectorfunctionintheacutephaseofdisease.ItwasdemonstratedthatSDRissufficienttoalterinflammation.ExposuretoasinglesessionofSDRincreasesIL-??1?mRNAexpression;however,IL-??6mRNAexpression,butnotIL-??1?,isupregulatedinresponsetochronicSDR.Furthermore,chronicSDRpriortoinfectionresultedinincreasedinfectionrelatedcentralIL-??6andIL-??1?mRNAexpression,andcentral administrationofIL-??6neutralizingantibodyduringSDRreversesthisincreaseinneuroinflammation.ThissuggeststhatSDRsensitizesinfectionrelatedCNSinflammationthroughanup-??regulationofIL-??6.ChronicSDRpriortoinfectionalsoresultedinenhancedCNSviraltitersandsuppressionofvirus-??inducedCD4 andCD8 TcellIFN-???releasewithintheCNS.Asawhole,thisresearchindicatesthatSDRexacerbatesthediseasecourseofTMEVinfectionbyalteringthecentralinnateandadaptiveimmuneresponsetoinfection.Thisresearchenhancesourunderstandingofthemechanismsbywhichsocialstressexacerbatesneurodegenerativediseasepathogenesis.
机译:Agrowingbodyofevidencesuggeststhatsocialstresscontributestothepathogenesisofneurodegenerativediseases,suchasmultiplesclerosis(MS).Forexample,priorresearchhasshownthatsocialdisruption(SDR)stressbehaviorallyandimmunologicallyexacerbatesTheiler smurineencephalomyelitisvirus(TMEV)infection.TMEVinfectionresultsinacuteinfectionofthecentralnervoussystem(CNS)followedbyachronicdemyelinatingautoimmunedisease,similartothatseeninMS.Researchsuggeststhatsocialstressexertstheseeffectsbyalteringtheimmuneresponsetoinfection.Morespecifically,itishypothesizedthatSDRsensitizestheacuteinflammatoryresponsetoinfectionandsuppressesTcelleffectorfunctionintheacutephaseofdisease.ItwasdemonstratedthatSDRissufficienttoalterinflammation.ExposuretoasinglesessionofSDRincreasesIL - α1 mRNA表达;然而,IL-?响应性慢性SDR上调了6mRNA的表达,但没有调节IL-1的表达。此外,感染前的慢性SDR导致与中央IL-6的表达增加有关的感染,IL-1β1的mRNA表达和IL-6的集中管理。 neutralizingantibodyduringSDRreversesthisincreaseinneuroinflammation.ThissuggeststhatSDRsensitizesinfectionrelatedCNSinflammationthroughanup - ?? regulationofIL - ?? 6.ChronicSDRpriortoinfectionalsoresultedinenhancedCNSviraltitersandsuppressionofvirus - ?? inducedCD4 andCD8 TcellIFN - ??? releasewithintheCNS.Asawhole,thisresearchindicatesthatSDRexacerbatesthediseasecourseofTMEVinfectionbyalteringthecentralinnateandadaptiveimmuneresponsetoinfection.Thisresearchenhancesourunderstandingofthemechanismsbywhichsocialstressexacerbatesneurodegenerativediseasepathogenesis。

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    Vichaya Elisabeth Good;

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  • 年度 2011
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