Proinflammatory and Th2 Cytokines Regulate the High Affinity IgE Receptor (FcεRI) and IgE-Dependant Activation of Human Airway Smooth Muscle Cells 英文参考文献.docVIP

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Proinflammatory and Th2 Cytokines Regulate the High Affinity IgE Receptor (FcεRI) and IgE-Dependant Activation of Human Airway Smooth Muscle Cells 英文参考文献.doc

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Proinflammatory and Th2 Cytokines Regulate the High Affinity IgE Receptor (FcεRI) and IgE-Dependant Activation of Human Airway Smooth Muscle Cells 英文参考文献

ProinflammatoryandTh2CytokinesRegulatetheHigh AffinityIgEReceptor(FceRI)andIgE-Dependant ActivationofHumanAirwaySmoothMuscleCells NareshSinghRedhu1,AliSaleh1,LianyuShan1,WilliamT.Gerthoffer2,SamK.Kung1,AndrewJ. Halayko3,BouchaibLamkhioued4,AbdelilahS.Gounni1* 1DepartmentofImmunology,SectionofRespiratoryDiseases,UniversityofManitoba,Winnipeg,Manitoba,Canada,2DepartmentofBiochemistryMolecularBiology, CollegeofMedicine,UniversityofSouthAlabama,Mobile,Alabama,UnitedStatesofAmerica,3DepartmentofPhysiology,SectionofRespiratoryDiseases,Universityof Manitoba,Winnipeg,Manitoba, Canada,4Laboratoired’ImmunologieetMicrobiologie, UFRdePharmaciedeReims‘EA4303,IFR53’Universite′ deReimsChampagne- Ardenne,Reims,France Abstract Background: The high affinity IgE receptor (FceRI) is a crucial structure for IgE-mediated allergic reactions. We have previously demonstrated that human airway smooth muscle (ASM) cells express the tetrameric (abc2) FceRI, and its activationleadstomarkedtransientincreasesinintracellularCa2+concentration,releaseofTh-2cytokinesandeotaxin-1/ CCL11.Therefore,itwasofutmostimportancetodelineatethefactorsregulatingtheexpressionofFceRIinhuman(ASM) cells. Methodology/PrincipalFindings:Incubationofhumanbronchialandtrachealsmoothmuscle(B/TSM)cellswithTNF-a ,IL- 1borIL-4resultedinasignificantincreaseinFceRI-achainmRNAexpression(p,0.05);andTNF-a,IL-4enhancedtheFceRI-a protein expression compared to the unstimulated control at 24, 72hrs after stimulation. Interestingly, among all other cytokines,onlyTNF-aupregulatedtheFceRI-cmRNAexpression.FceRI-cproteinexpressionremainedunchangeddespite the nature of stimulation. Of note, as a functional consequence of FceRI upregulation, TNF-a pre-sensitization of B/TSM potentially augmented the CC (eotaxin-1/CCL11 and RANTES/CCL5, but not TARC/CCL17) and CXC (IL-8/CXCL8, IP-10/ CXCL10) chemokines release following IgE stimulation (p,0.05, n=3). Furthermore, IgE sensitization of B/TSM cells significantlyenhancedthetranscriptiono