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JNeurolSci.1997Nov25152(2):11924.
GeneexpressionofIL10inrelationshiptoTNFalpha,IL1betaandIL2
intheratbrainfollowingmiddlecerebralarteryocclusion.
ZhaiQH1,FutrellN,ChenFJ.
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Abstract
Tosystematicallyelucidatethegeneexpressionofinflammatoryandimmunemodulatorsfollowing
middlecerebralarteryocclusion(MCAO)intherat,westudiedinterleukin10(IL10)alongwith
tumornecrosisfactoralpha(TNFalpha),interleukin1beta(IL1beta)andinterleukin2(IL2).
GeneexpressionofthesecytokineswasstudiedipsilateralandcontralateraltotheMCAO,with
mRNAexpressionlevelsevaluated2,4,6,8and12hfollowingpermanentMCAObyreverse
transcriptasepolymerasechainreaction(RTPCR).IntheischemichemisphereTNFalphaandIL
1betamRNAincreasedat2hfollowingMCAOandpeakedat6h,withIL10mRNAdetectedonly
at6h.Contralaterally,bothTNFalphaandIL1betamRNAswereexpressedwithasimilarpattern
tothatintheischemichemisphere,butatlowerlevels,withnocontralateralIL10expression.
TherewasnodifferenceinIL2geneexpressionbetweencontrolandexperimentalanimalsin
eitherhemisphere.TheseresultsdemonstratethatIL10andTNFalpha,IL1betagene
expressionisinducedearlyfollowingMCAO.Thetemporalprofileofthesecytokinesissimilarto
thatseeninsepsis,whereTNFalphainducesIL10subsequentlyIL10inhibitsTNFalpha
expression.Thesimilarityofthetemporalprofileofcytokineexpressioninsepsisandcerebral
ischemiasuggeststhatIL10shouldbestudiedasapotentialinhibitorofTNFalphaproductionin
ischemicbraintissue.Thefactorsinducingcontralateralexpressionoftheinflammatorycytokines,
TNFalphaandIL1beta,alongwiththepotentialclinicalsignificanceofthisremotecytokinegene
expression,meritfurtherstudy.
PMID:9415530[PubMedindexedforMEDLINE]
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http://www.ncbi.nlm.nih.gov/pubmed/9415530 1/2
4/5/2016 GeneexpressionofIL10inrelationshiptoTNFalpha,IL1betaandIL2intheratbrainfollowingmiddlecerebralarteryocclusion.PubMedNCBI
http://www.ncbi.nlm.nih.gov/pubmed/9415530 2/2