Activation of Epidermal Growth Factor Receptor Is Required for NTHi-Induced NF-κB-Dependent Inflammation 英文参考文献.docVIP

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Activation of Epidermal Growth Factor Receptor Is Required for NTHi-Induced NF-κB-Dependent Inflammation 英文参考文献.doc

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Activation of Epidermal Growth Factor Receptor Is Required for NTHi-Induced NF-κB-Dependent Inflammation 英文参考文献

ActivationofEpidermalGrowthFactorReceptorIs RequiredforNTHi-InducedNF-kB-Dependent Inflammation XiangbinXu1*,RachelR.Steere1,ChristineA.Fedorchuk1,JinjiangPang2,Ji-YunLee1,3,JaeHyang Lim1,3,HaidongXu1,3,ZhixingK.Pan4,SanjayB.Maggirwar1,Jian-DongLi1,3* 1DepartmentofMicrobiologyandImmunology,UniversityofRochesterMedicalCenter,Rochester,NewYork,UnitedStatesofAmerica,2AabCardiovascularResearch Institute, University of Rochester Medical Center, Rochester, New York, United States of America, 3Department of Biology, Center for Inflammation, Immunity and Infection, Georgia State University, Atlanta, Georgia, United States of America, 4Department of Medical Microbiology and Immunology, University of Toledo Medical Center,Toledo,Ohio,UnitedStatesofAmerica Abstract Background:Inflammationisahallmarkofmanyserioushumandiseases.NontypeableHaemophilusinfluenzae(NTHi)isan important human pathogen causing respiratory tract infections in both adults and children. NTHi infections are characterized by inflammation, which is mainly mediated by nuclear transcription factor-kappa B (NF-kB)-dependent productionofproinflammatorymediators.Epidermalgrowthfactorreceptor(EGFR)hasbeenshowntoplayimportantroles inregulatingdiversebiologicalprocesses,includingcellgrowth,differentiation,apoptosis,adhesion,andmigration.Itsrole inregulatingNF-kBactivationandinflammation,however,remainslargelyunknown. Methodology/Principal Findings: In the present study, we demonstrate that EGFR plays a vital role in NTHi-induced NF-kB activation and the subsequent induction of proinflammatory mediators in human middle ear epithelial cells and othercelltypes.Importantly,wefoundthatAG1478,aspecifictyrosinekinaseinhibitorofEGFRpotentlyinhibitedNTHi- inducedinflammatoryresponsesinthemiddleearsandlungsofmiceinvivo.Moreover,wefoundthatMKK3/6-p38and PI3K/AktsignalingpathwaysarerequiredformediatingEGFR-dependentNF-kBactivationandinflammatoryresponsesby NTHi. Conclusions/Significance:Here,weprovidedirectevidencethatEGFRplaysa