Phagocytic Superoxide Specifically Damages an Extracytoplasmic Target to Inhibit or Kill Salmonella 英文参考文献.docVIP
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Phagocytic Superoxide Specifically Damages an Extracytoplasmic Target to Inhibit or Kill Salmonella 英文参考文献
PhagocyticSuperoxideSpecificallyDamagesan
ExtracytoplasmicTargettoInhibitorKillSalmonella
MaureenCraig1,JamesM.Slauch1,2*
1DepartmentofMicrobiology,UniversityofIllinois,Urbana,Illinois,UnitedStatesofAmerica,2CollegeofMedicine,UniversityofIllinois,Urbana,Illinois,UnitedStatesof
America
Abstract
Background: The phagocytic oxidative burst is a primary effector of innate immunity that protects against bacterial
infection.However,themechanismbywhichreactiveoxygenspecies(ROS)killorinhibitbacteriaisnotknown.Itisoften
assumedthatDNAisaprimarytargetofoxidativedamage,consistentwithknowneffectsofendogenouslyproducedROS
inthebacterialcytoplasm.ButmoststudiesfailtodistinguishbetweeneffectsofhostderivedROSversusdamagecaused
by endogenous bacterial sources. We took advantage of both the ability of Salmonella enterica serovar Typhimurium to
survive in macrophages and the genetic tractability of the system to test the hypothesis that phagocytic superoxide
damagescytoplasmictargetsincludingDNA.
Methodology/PrincipalFindings:SodCIisaperiplasmicCu-Znsuperoxidedismutase(SOD)thatcontributestothesurvival
of Salmonella Typhimurium in macrophages. Through competitive virulence assays, we asked if sodCI has a genetic
interaction with various cytoplasmic systems. We found that SodCI acts independently of cytoplasmic SODs, SodA and
SodB.Inaddition,SodCIactsindependentlyofthebaseexcisionrepairsystemandRuvAB,involvedinDNArepair.Although
sodCIdidshowgeneticinteractionwithrecA,thiswasapparentlyindependentofrecombinationandispresumablydueto
thepleiotropiceffectsofarecAmutation.
Conclusions/Significance: Taken together, these results suggest that bacterial inhibition by phagocytic superoxide is
primarilytheresultofdamagetoanextracytoplasmictarget.
Citation:CraigM,SlauchJM(2009)PhagocyticSuperoxideSpecificallyDamagesanExtracytoplasmicTargettoInhibitorKillSalmonella.PLoSONE4(3):e4975.
doi:10.1371/journal.pone.0004975
Editor:FrederickM.Ausubel,MassachusettsGeneralHospital,UnitedStatesofAmerica
Receiv
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