Cigarette Smoke Decreases Airway Epithelial FABP5 Expression and Promotes Pseudomonas aeruginosa Infection.docVIP

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Cigarette Smoke Decreases Airway Epithelial FABP5 Expression and Promotes Pseudomonas aeruginosa Infection.doc

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Cigarette Smoke Decreases Airway Epithelial FABP5 Expression and Promotes Pseudomonas aeruginosa Infection

CigaretteSmokeDecreasesAirwayEpithelialFABP5 ExpressionandPromotesPseudomonasaeruginosa Infection FabienneGally,HongWeiChu,RussellP.Bowler* PulmonaryDivision,DepartmentofMedicine,NationalJewishHealth,Denver,Colorado,UnitedStatesofAmerica Abstract CigarettesmokingistheprimarycauseofChronicObstructivePulmonaryDisease(COPD),whichischaracterizedbychronic inflammationoftheairwaysanddestructionoflungparenchyma.Repeatedandsustainedbacterialinfectionsareclearly linked to disease pathogenesis (e.g., exacerbations) and a huge burden on health care costs. The airway epithelium constitutesthefirstlineofhostdefenseagainstinfectionandourpreviousstudyindicatedthatFattyAcidBindingProtein5 (FABP5) is down regulated in airway epithelial cells of smokers with COPD as compared to smokers without COPD. We hypothesized that cigarette smoke (CS) exposure down regulates FABP5, thus, contributing to a more sustained inflammationinresponsetobacterialinfection.Inthisreport,weshowthatFABP5isincreasedfollowingbacterialinfection butdecreasedfollowingCSexposureofprimarynormalhumanbronchialepithelial(NHBE)cells.Thegoalofthisstudywas to address FABP5 function by knocking down or overexpressing FABP5 in primary NHBE cells exposed to CS. Our data indicatethatFABP5downregulationresultsinincreasedP.aeruginosabacterialloadandinflammatorycytokinelevels(e.g., IL-8)anddecreasedexpressionoftheanti-bacterialpeptide,bdefensin-2.Onthecontrary,FABP5overexpressionexertsa protectivefunctioninairwayepithelialcellsagainstP.aeruginosainfectionbylimitingtheproductionofIL-8andincreasing the expression of b defensin-2. Our study indicates that FABP5 exerts immunomodulatory functions in the airway epithelium against CS exposure and subsequent bacterial infection through its modulation of the nuclear receptor peroxisome proliferator-activated receptor (PPAR)-c activity. These findings support the development of FABP5/PPAR-c- targeted therapeutic approach to prevent airway inflammation by restoring antimicrobial immunit