An Altered Immune Response, but Not Individual Cationic Antimicrobial Peptides, Is Associated with the Oral Attenuation of Ara4N-Deficient Salmonella enterica Serovar Typhimurium in Mice 英文参考文献.docVIP

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An Altered Immune Response, but Not Individual Cationic Antimicrobial Peptides, Is Associated with the Oral Attenuation of Ara4N-Deficient Salmonella enterica Serovar Typhimurium in Mice 英文参考文献.doc

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AnAlteredImmuneResponse,butNotIndividual CationicAntimicrobialPeptides,IsAssociatedwiththe OralAttenuationofAra4N-DeficientSalmonellaenterica SerovarTyphimuriuminMice KristiL.Strandberg1.,SusanM.Richards1.,RitaTamayo2,LinhT.Reeves2,JohnS.Gunn1,2* 1CenterforMicrobialInterfaceBiology,TheOhioStateUniversity,Columbus,Ohio,UnitedStatesofAmerica,2DepartmentofMicrobiologyandImmunology,University ofTexasHealthScienceCenteratSanAntonio,SanAntonio,Texas,UnitedStatesofAmerica Abstract SalmonellaentericaserovarTyphimurium(S.Typhimurium)usestwo-componentregulatorysystems(TCRS)torespondto stimuliinthelocalmicroenvironment.Uponinfection,theSalmonellaTCRSsPhoP-PhoQ(PhoPQ)andPmrA-PmrB(PmrAB) areactivatedbyenvironmentalsignalsintheintestinallumenandwithinhostcells.TCRS-mediatedgeneexpressionresults in lipopolysaccharide (LPS) modification and cationic antimicrobial peptide resistance. The PmrA-regulated pmrHFIJKLM operon mediates 4-amino-4-deoxy-L-arabinose (Ara4N) production and attachment to the lipid A of LPS. A DpmrF S. TyphimuriumstraincannotproduceAra4N,exhibitsincreasedsensitivitytocationicantimicrobialpeptide(CAMP)-mediated killing,andattenuatedvirulenceinmiceuponoralinfection.CAMPsarepredictedtoplayaroleineliminationofSalmonella, and may activate PhoPQ and PmrAB invivo, which could increase bacterial resistance to host defenses. Competition experiments between wild type (WT) and DpmrF mutant strains of S. Typhimurium indicated that selection against this mutantfirstoccurswithintheintestinallumenearlyduringinfection.However,CRAMPandactivecryptdinsalonearenot responsible for elimination of Ara4N-deficient bacteria invivo. Investigation into the early immune response to DpmrF showedthatitdifferedslightlyfromtheearlyimmuneresponsetoWTS.Typhimurium.Furtherinvestigationintotheearly immuneresponsetoinfectionofPeyer’spatchessuggestsaroleforIL-13intheattenutionofthe DpmrFmutantstrain. Thus,prominentCAMPspresentinthemouseintestinearenotresponsiblefortheselectionagainsttheD