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Neutrophils infected with highly virulent influenza H3N2 virus exhibit augmented early cell death and rapid induction of type I interferon signaling pathways

机译:感染高毒力H3N2流感病毒的中性粒细胞显示出早期细胞死亡增加和I型干扰素信号传导途径的快速诱导

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WedevelopedamodelofinfluenzavirusinfectionofneutrophilsbyinducingdifferentiationoftheMPROpromyelocyticcellline.After5#xA0;daysofdifferentiation,about20ndash;30%ofmatureneutrophilscouldbedetected.Onlyafractionofneutrophilswereinfectedbyhighlyvirulentinfluenza(HVI)virus,butwereunabletosupportactiveviralreplicationcomparedwithMDCKcells.HVIinfectionofneutrophilsaugmentedearlyandlateapoptosisasindicatedbyannexinVandTUNELassays.ComparisonbetweentheglobaltranscriptomicresponsesofneutrophilstoHVIandlowvirulentinfluenza(LVI)revealedthattheIFNregulatoryfactorandIFNsignalingpathwayswerethemostsignificantlyoverrepresentedpathways,withactivationofrelatedgenesinHVIasearlyas3#xA0;h.Relativelyconsistentresultswereobtainedbyreal-timeRT-PCRofselectedgenesassociatedwiththetypeIIFNpathway.EarlyafterHVIinfection,comparativelyenhancedexpressionofapoptosis-relatedgeneswasalsoelicited./p/div
机译:WedevelopedamodelofinfluenzavirusinfectionofneutrophilsbyinducingdifferentiationoftheMPROpromyelocyticcellline.After5#XA0; daysofdifferentiation,about20ndash; 30%ofmatureneutrophilscouldbedetected.Onlyafractionofneutrophilswereinfectedbyhighlyvirulentinfluenza(HVI)病毒,butwereunabletosupportactiveviralreplicationcomparedwithMDCKcells.HVIinfectionofneutrophilsaugmentedearlyandlateapoptosisasindicatedbyannexinVandTUNELassays.ComparisonbetweentheglobaltranscriptomicresponsesofneutrophilstoHVIandlowvirulentinfluenza(LVI)revealedthattheIFNregulatoryfactorandIFNsignalingpathwayswerethemostsignificantlyoverrepresentedpathways,withactivationofrelatedgenesinHVIasearlyas3#XA0; h.Relativelyconsistentresultswereobtainedbyreal-timeRT-PCRofselectedgenesassociatedwiththetypeIIFNpathway.EarlyafterHVIinfection,comparativelyenhancedexpressionofapoptosis-relatedgeneswasalsoelicited

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