Analysis of Pulmonary Inflammation and Function in the Mouse and Baboon after Exposure to Mycoplasma pneumoniae CARDS Toxin 英文参考文献.docVIP
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Analysis of Pulmonary Inflammation and Function in the Mouse and Baboon after Exposure to Mycoplasma pneumoniae CARDS Toxin 英文参考文献
AnalysisofPulmonaryInflammationandFunctioninthe
MouseandBaboonafterExposuretoMycoplasma
pneumoniaeCARDSToxin
R.DougHardy4,6,JacquelineJ.Coalson3,5,JayPeters2,5,AdrianaChaparro1,5 ,Chonnamet
Techasaensiri4,6,AngeleneM.Cantwell1,5,T.R.Kannan1,5,JoelB.Baseman1,5,PeterH.Dube1,5
*
1DepartmentofMicrobiologyandImmunology,UniversityofTexasHealthSciencesCenteratSanAntonio,SanAntonio,Texas,UnitedStatesofAmerica,2Department
ofMedicine,DivisionofPulmonaryandCriticalCareMedicine,UniversityofTexasHealthSciencesCenteratSanAntonio,SanAntonio,Texas,UnitedStatesofAmerica,
3DepartmentofPathology,UniversityofTexasHealthSciencesCenteratSanAntonio,SanAntonio,Texas,UnitedStatesofAmerica,4DepartmentofInternalMedicine
andPediatricInfectiousDiseases,UniversityofTexasHealthSciencesCenteratSanAntonio,SanAntonio,Texas,UnitedStatesofAmerica,5UniversityofTexasHealth
SciencesCenteratSanAntonio,SanAntonio,Texas,UnitedStatesofAmerica,6UniversityofTexasSouthwesternMedicalCenter,Dallas,Texas,UnitedStatesofAmerica
Abstract
MycoplasmapneumoniaeproducesanADP-ribosylatingandvacuolatingtoxinknownastheCARDS(CommunityAcquired
RespiratoryDistressSyndrome)toxinthathasbeenshowntobecytotoxictomammaliancellsintissueandorganculture.In
thisstudywetestedtheabilityofrecombinantCARDS(rCARDS)toxintoelicitchangeswithinthepulmonarycompartment
inbothmiceandbaboons.AnimalsrespondedtoarespiratoryexposuretorCARDStoxininadoseandactivity-dependent
mannerbyincreasingtheexpressionofthepro-inflammatorycytokinesIL-1a,1b,6,12,17,TNF-aandIFN-c.Therewasalso
adose-dependentincreaseinseveralgrowthfactorsandchemokinesfollowingtoxinexposureincludingKC,IL-8,RANTES,
andG-CSF.IncreasedexpressionofIFN-cwasobservedonlyinthebaboon;otherwise,miceandbaboonsrespondedto
CARDStoxininaverysimilarmanner.IntroductionofrCARDStoxintotheairwaysofmiceorbaboonsresultedinacellular
inflammatory response characterized by a dose-dependent early vacuolization and cytotoxicity of the bronchiolar
epitheliumfollowedbyarobustperibronchialandperivascularlymphocyti
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