A Modeling-Derived Hypothesis on Chronicity in Respiratory Diseases Desensitized Pathogen Recognition Secondary to Hyperactive IRAKTRAF6 Signaling 英文参考文献.docVIP

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A Modeling-Derived Hypothesis on Chronicity in Respiratory Diseases Desensitized Pathogen Recognition Secondary to Hyperactive IRAKTRAF6 Signaling 英文参考文献.doc

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A Modeling-Derived Hypothesis on Chronicity in Respiratory Diseases Desensitized Pathogen Recognition Secondary to Hyperactive IRAKTRAF6 Signaling 英文参考文献

AModeling-DerivedHypothesisonChronicityin RespiratoryDiseases:DesensitizedPathogen RecognitionSecondarytoHyperactiveIRAK/TRAF6 Signaling TingtingZhang*,KyungW.Song,MohammadHekmat-Nejad,DavidG.Morris,BrianR.Wong RochePaloAltoLLC,PaloAlto,California,UnitedStatesofAmerica Abstract Severalchronicrespiratorydiseasesexhibithyperactiveimmuneresponsesinthelung:abundantinflammatorymediators; infiltratingneutrophils,macrophages,lymphocytesandotherimmunecells;andincreasedlevelofproteases.Suchdiseases include cystic fibrosis (CF), chronic obstructive pulmonary disease (COPD) and severe/neutrophilic asthma. Paradoxically, patientswiththesediseasesarealsosusceptibletodetrimentalbacterialinfectionandcolonization.Inthispaper,weseekto explainhowapositivefeedbackmechanismviaIL-8couldleadtodesensitizationofepithelialcellstopathogenrecognition thus perpetuating bacterial colonization and chronic disease states in the lung. Such insight was obtained from mathematicalmodelingoftheIRAK/TRAF6signalingmodule,andisconsistentwithexistingclinicalevidence.Thepotential implicationsfortargetedtreatmentregimesforthesepersistentrespiratorydiseasesareexplored. Citation:ZhangT,SongKW,Hekmat-NejadM,MorrisDG,WongBR(2009)AModeling-DerivedHypothesisonChronicityinRespiratoryDiseases:Desensitized PathogenRecognitionSecondarytoHyperactiveIRAK/TRAF6Signaling.PLoSONE4(4):e5332.doi:10.1371/journal.pone.0005332 Editor:NeerajVij,JohnsHopkinsSchoolofMedicine,UnitedStatesofAmerica ReceivedDecember23,2008;AcceptedMarch30,2009;PublishedApril24,2009 Copyright: ? 2009 Zhang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecredited. Funding:Theauthorshavenosupportorfundingtoreport. CompetingInterests:Theauthorshavedeclaredthatnocompetinginterestsexist. *E-mail:tingting.zhang@ Introduction IRAK module has been reported [3], and neutrophil elastase prod