Azithromycin Treatment Alters Gene Expression in Inflammatory, Lipid Metabolism, and Cell Cycle Pathways in Well-Differentiated Human Airway Epithelia 英文参考文献.docVIP

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Azithromycin Treatment Alters Gene Expression in Inflammatory, Lipid Metabolism, and Cell Cycle Pathways in Well-Differentiated Human Airway Epithelia 英文参考文献.doc

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Azithromycin Treatment Alters Gene Expression in Inflammatory, Lipid Metabolism, and Cell Cycle Pathways in Well-Differentiated Human Airway Epithelia 英文参考文献

AzithromycinTreatmentAltersGeneExpressionin Inflammatory,LipidMetabolism,andCellCyclePathways inWell-DifferentiatedHumanAirwayEpithelia CarlaMariaP.Ribeiro1,2*,HarryHurd3,YichaoWu3¤,MaryE.B.Martino1,LisaJones1,BrianBrighton1, RichardC.Boucher1,2,WandaK.O’Neal1,2 1CysticFibrosisCenter,TheUniversityofNorthCarolinaatChapelHill,ChapelHill,NorthCarolina,UnitedStateofAmerica,2DepartmentofMedicine,TheUniversityof NorthCarolinaatChapelHill,ChapelHill,NorthCarolina,UnitedStateofAmerica,3DepartmentofStatistics,TheUniversityofNorthCarolinaatChapelHill,ChapelHill, NorthCarolina,UnitedStateofAmerica Abstract Prolonged macrolide antibiotic therapy at low doses improves clinical outcome in patients affected with diffuse panbronchiolitisandcysticfibrosis.Consensusisbuildingthatthetherapeuticeffectsareduetoanti-inflammatory,rather thananti-microbialactivities,butthemodeofactionislikelycomplex.Togaininsightsintohowthemacrolideazithromycin (AZT) modulates inflammatory responses in airways, well-differentiated primary cultures of human airway epithelia were exposedtoAZTalone,aninflammatorystimulusconsistingofsolublefactorsfromcysticfibrosisairways,orAZTfollowedby the inflammatory stimulus. RNA microarrays were conducted to identify global and specific gene expression changes. AnalysisofgeneexpressionchangesrevealedthattheAZTtreatmentalonealteredthegeneprofileofthecells,primarilyby significantlyincreasingtheexpressionoflipid/cholesterolgenesanddecreasingtheexpressionofcellcycle/mitosisgenes. Theincreaseincholesterolbiosyntheticgeneswasconfirmedbyincreasedfilipinstaining,anindexoffreecholesterol,after AZTtreatment.AZTalsoaffectedgeneswithinflammatoryannotations,buttheeffectwasvariable(bothup-anddown- regulation)andgenespecific.AZTpretreatmentpreventedtheup-regulationofsomegenes,suchasMUC5ACandMMP9, triggeredbytheinflammatorystimulus,buttheup-regulationofotherinflammatorygenes,e.g.,cytokinesandchemokines, suchasinterleukin-8,wasnotaffected.Ontheotherhand,HLAgeneswereincreasedbyAZT.Notab