Alternaria-Induced Release of IL-18 from Damaged Airway Epithelial Cells An NF-κB Dependent Mechanism of Th2 Differentiation 英文参考文献.docVIP

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Alternaria-Induced Release of IL-18 from Damaged Airway Epithelial Cells An NF-κB Dependent Mechanism of Th2 Differentiation 英文参考文献.doc

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Alternaria-Induced Release of IL-18 from Damaged Airway Epithelial Cells An NF-κB Dependent Mechanism of Th2 Differentiation 英文参考文献

Alternaria-InducedReleaseofIL-18fromDamaged AirwayEpithelialCells:AnNF-kBDependentMechanism ofTh2Differentiation? HirokiMurai1.,HuibinQi1.,BarunChoudhury1.,JimWild1,NileshDharajiya1,SwapnilVaidya1 ,Anjana Kalita1,AttilaBacsi1,DavidCorry2,AlexanderKurosky3,AllanBrasier1,IstvanBoldogh4,SanjivSur1* 1DepartmentofInternalMedicine,UniversityofTexasMedicalBranch,Galveston,Texas,UnitedStatesofAmerica,2DivisionofPulmonaryandCriticalCare,Department of Medicine, Baylor College of Medicine, Houston, Texas, United States of America, 3Department of Biochemistry and Molecular Biology, University of Texas Medical Branch,Galveston,Texas,UnitedStatesofAmerica,4DepartmentofMicrobiology,UniversityofTexasMedicalBranch,Galveston,Texas,UnitedStatesofAmerica Abstract Background:AseriesofepidemiologicstudieshaveidentifiedthefungusAlternariaasamajorriskfactorforasthma.The airwayepitheliumplaysacriticalroleinthepathogenesisofallergicasthma.Thesereportssuggestthatactivatedairway epithelialcellscanproducecytokinessuchasIL-25,TSLPandIL-33thatinduceTh2phenotype.Howevertheepithelium- derived products that mediate the pro-asthma effects of Alternaria are not well characterized. We hypothesized that exposureoftheairwayepitheliumtoAlternariareleasingcytokinesthatcaninduceTh2differentiation. Methodology/PrincipalFinding:WeusedELISAtomeasurehumanandmousecytokines.Alternariaextract(ALT-E)induced rapidreleaseofIL-18,butnotIL-4,IL-9,IL-13,IL-25,IL-33,orTSLPfromculturednormalhumanbronchialepithelialcells;and in the BAL fluids of na?¨ve mice after challenge with ALT-E. Both microscopic and FACS indicated that this release was associated with necrosis of epithelial cells. ALT-E induced much greater IL-18 release compared to 19 major outdoor allergens.Cultureofna?¨veCD4cellswithrmIL-18inducedTh2differentiationintheabsenceofIL-4andSTAT6,andthis effectwasabrogatedbydisruptingNF-kBp50orwithaNEMObindingpeptideinhibitor. Conclusion/Significance: RapidandspecificreleaseofIL-18fromAlternaria-exposeddamagedairwayep