简介：

简介：

简介：

简介：

简介：

简介：TheexpressionofIL-4inaratmodelofchronicpulmonaryinfectionbiofilmformationinducedbyPseudomonasaeruginosawasinvestigated,inwhichSPFWisterratswereinfectedviatracheawith0.1mlP.aeruginosastrainPAO579(10~9CFU/ml)inalginatebeadsortheplanktonicformofthisbacterialstrain(10~9CFU/ml),andon3,7and14dafterinfection,thebacteriologicalandpathologicalchangeswereobservedaswellastheexpressionofthecytokineIL-4wasdetermined.ItwasdemonstratedthatthecountofCFUperlungtissueincaseofbacteriainalginatebeadswassignificantlyhigherthanthatofbacteriainplanktonicform,withmoreseveregrosspathologicchangesandinflammatoryreactionsinthealginatebeadgroupincomparisonwiththatoftheplanktonicforms(P=0.002,P=0.004andP=0.002,respectively).Inaddition,theexpressionofIL-4inthealginatebeadgroupwasalsohigherthanthatintheplanktonicform(P=0.02,P=0.02andP=0.022,respectively).Apositivecorre-lationbetweenthelevelofIL-4expressionandthegrosslungpathologyinalginatebeadgroupexistedasdemonstratedbysimpleregressionanalysis(r=0.78,P<0.02).Itisconcludedthatthechronicpul-monaryinfectionwithbiofilmformationinducedbyP.aeruginosatendstohavetheprioritytotheTh2immuneresponse.

简介：

简介：

简介：

简介：InordertoinvestigatewhetherlipoxinA4(LXA4)hasanantagonisticeffectonlipopolysaccharide(LPS)-inducedsynthesisofinterleukin(IL)-1β,IL-6andIL-8inratpulmonarymicrovascularendothelialcells(PMVEC),andtoexplorethemolecularmechanismsofsignalpathwayinLXA4actions,culturedPMVECweretreatedwithLPS,withorwithoutpreincubationwithLXA4.ProteinsofIL-1β,IL-6andIL-8insupernatantwereanalyzedbyenzyme-linkedimmunosorbentassay(ELISA).ExpressionsofmRNAofIL-1β,IL-6andIL-8weredeterminedbyRT-PCR.Expressionsofphosphorylationofphosphoinositide3-kinase(PI3-K)andmyeloiddifferentiationfactor88(MyD88)wereanalyzedbyWesternblot.ActivitiesofDNA-bindingofnuclearfactor-kappaB(NF-κB)andactivatorprotein-1(AP-1)weremeasuredbyelectrophoreticmobilityshiftassay(EMSA).TheresultsshowedthatLPSinducedproductionofIL-1β,IL-6andIL-8inratPMVECviaMyD88/PI3-K/NF-κBandAP-1pathway-dependentsignaltransduction.LPS-stimulatedexpressionofPI3-K,activitiesofNFκBandAP-1,secretionofproteinandexpressionofmRNAofIL-1β,IL-6andIL-8butnotMyD88expressioninPMVECwereinhibitedbyLXA4inadose-dependentmanner.Inconclusion,LXA4inhibitssynthesisofIL-1β,IL-6andIL-8bydown-regulationofPI3-K/NF-κBandAP-1signalpathwayinPMVEC.

简介：

简介：

简介：ExposureofnaivemurineCD4^+TlymphocytestosuperantigensuchasstaphylococcalenterotoxinB(SEB)inducesastrongproliferativeresponse.ProlongedexposureorsubsequentrestimulationoftherespondingTcellpopulationwithSEBleadstotheapoptoticeventsofactivation-inducedcelldeath(AICD).ThesignalingmechanismresponsiblefortheAICDisatargetofintensiveinvestigation.However,theprecisedownstreamsignahngpathwaysofSEB-inducedAICDremainsunclear.Ourresultshereshowthatthesequentialactivationofcaspase-1/ICE-hkeandcaspase-3/CPP32-hkecysteineproteasesprobablyplaysaroleinthesignalingtransductionofSEB-inducedAICD,butcaspase-3/CPP32-hkeproteasesactivationdoesnotdependoncaspase-1-likeproteasesactivation.HerbimycinA,aspecificinhibitorofproteintyresinekinases,inhibitcaspase-3/CPP32-1ikecysteineproteasesactivation.However,itdoesnotpreventDNAfragmentationofCD4^+TcellsapoptosisinducedbySEB.TheseresultsindicatethatproteintyrosinekinasespathwayisprobablyinvolvedinthesignalingtransductionofCD4^+TcellsapoptosisinducedbySEBand“crosstalks”withthepathwayofcaspase-3/CPP32-1ikeproteasesactivation.