Carbon Monoxide Blocks Lipopolysaccharide-Induced Gene Expression by Interfering with Proximal TLR4 to NF-κB Signal Transduction in Human Monocytes 英文参考文献.docVIP

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Carbon Monoxide Blocks Lipopolysaccharide-Induced Gene Expression by Interfering with Proximal TLR4 to NF-κB Signal Transduction in Human Monocytes 英文参考文献.doc

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Carbon Monoxide Blocks Lipopolysaccharide-Induced Gene Expression by Interfering with Proximal TLR4 to NF-κB Signal Transduction in Human Monocytes 英文参考文献

CarbonMonoxideBlocksLipopolysaccharide-Induced GeneExpressionbyInterferingwithProximalTLR4to NF-kBSignalTransductioninHumanMonocytes ManeeshaChhikara1,ShuibangWang1,StevenJ.Kern1,GabrielaA.Ferreyra1,JenniferJ.Barb2,PeterJ. Munson2,RobertL.Danner1* 1CriticalCareMedicineDepartment,ClinicalCenter,NationalInstitutesofHealth,Bethesda,Maryland,UnitedStatesofAmerica,2MathematicalandStatisticalComputing Laboratory,CenterforInformationTechnology,NationalInstitutesofHealth,Bethesda,Maryland,UnitedStatesofAmerica Abstract Carbon monoxide (CO) is an endogenous messenger that suppresses inflammation, modulates apoptosis and promotes vascularremodeling.Here,microarrayswereemployedtogloballycharacterizetheCO(250ppm)suppressionofearly(1h) LPS-inducedinflammationinhumanmonocyticTHP-1cells.COsuppressed79of101immediate-earlygenesinducedby LPS;19%(15/79)weretranscriptionfactorsandmostotherswerecytokines,chemokinesandimmuneresponsegenes.The prototypiceffectsofCOontranscriptionandproteinproductionoccurredearlybutdecreasedrapidly.COactivatedp38 MAPK,ERK1/2andAktandcausedanearlyandtransitorydelayinLPS-inducedJNKactivation.However,selectiveinhibitors ofthesekinasesfailedtoblockCOsuppressionofLPS-inducedIL-1b,aninflammationmarker.OfCO-suppressedgenes,81% (64/79)werefoundtohavepromoterswithputativeNF-kBbindingsites.COwassubsequentlyshowntoblockLPS-induced phosphorylationanddegradationofIkBainhumanmonocytes,therebyinhibitingNF-kBsignaltransduction.CObroadly suppresses the initial inflammatory response of human monocytes to LPS by reshaping proximal events in TLR4 signal transductionsuchasstresskinaseresponsesandearlyNF-kBactivation.Theserapid,buttransienteffectsofCOmayhave therapeuticapplicationsinacutepulmonaryandvascularinjury. Citation:ChhikaraM,WangS,KernSJ,FerreyraGA,BarbJJ,etal.(2009)CarbonMonoxideBlocksLipopolysaccharide-InducedGeneExpressionbyInterfering withProximalTLR4toNF-kBSignalTransductioninHumanMonocytes.PLoSONE4(12):e8139.doi:10.1371/journal.pone.0008139 Editor:RamyK.Aziz,Cai