Exogenous HIV-1 Nef Upsets the IFN-γ-Induced Impairment of Human Intestinal Epithelial Integrity 英文参考文献.docVIP

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Exogenous HIV-1 Nef Upsets the IFN-γ-Induced Impairment of Human Intestinal Epithelial Integrity 英文参考文献.doc

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Exogenous HIV-1 Nef Upsets the IFN-γ-Induced Impairment of Human Intestinal Epithelial Integrity 英文参考文献

ExogenousHIV-1NefUpsetstheIFN-c-Induced ImpairmentofHumanIntestinalEpithelialIntegrity MariaGiovannaQuaranta1*,OlimpiaVincentini2,CristinaFelli1,FrancescaSpadaro3,MarcoSilano2, DiegoMoricoli4,LucianaGiordani1,MarinaViora1 1Department of Therapeutic Research and Medicine Evaluation, Istituto Superiore di Sanita`, Roma, Italy, 2Department of Veterinary Public Health and Food Safety, IstitutoSuperiorediSanita`, Roma,Italy,3DepartmentofCellBiologyandNeurosciences,IstitutoSuperiorediSanita`, Roma,Italy,4Diathevas.r.l.,Fano(PU),Italy Abstract Background:ThemucosaltissuesplayacentralroleinthetransmissionofHIV-1infectionaswellasinthepathogenesisof AIDS.DespiteseveralclinicalstudiesreportedintestinaldysfunctionduringHIVinfection,themechanismsunderlyingHIV- induced impairments of mucosal epithelial barrier are still unclear. It has been postulated that HIV-1 alters enterocytic function and HIV-1 proteins have been detected in several cell types of the intestinal mucosa. In the present study, we analyzedtheeffectoftheaccessoryHIV-1Nefproteinonhumanepithelialcellline. Methodology/PrincipalFindings:WeusedunstimulatedorIFN-c-stimulatedCaco-2cells,asamodelforhomeostaticand inflamed gastrointestinal tracts, respectively. We investigated the effect of exogenous recombinant Nef on monolayer integrityanalyzingitsuptake,transepithelialelectricalresistance,permeabilitytoFITC-dextranandtheexpressionoftight junctionproteins.Moreover,wemeasuredtheinductionofproinflammatorymediators.ExogenousNefwastakenupby Caco-2cells,increasedintestinalepithelialpermeabilityandupsettheIFN-c-inducedreductionoftransepitelialresistance, interferingwithtightjunctionproteinexpression.Moreover,NefinhibitedIFN-c-inducedapoptosisandup-regulatedTNF-a, IL-6andMIP-3aproductionbyCaco-2cellswhiledown-regulatedIL-10production.ThesimultaneousexposureofCaco-2 cellstoNefandIFN-cdidnotaffectcytokinesecretionrespecttountreatedcells.Finally,wefoundthatNefcounteracted theIFN-cinducedarachidonicacidcascade. Conclusion