Defects in Actin Dynamics Lead to an Autoinflammatory Condition through the Upregulation of CXCL5 英文参考文献.docVIP

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Defects in Actin Dynamics Lead to an Autoinflammatory Condition through the Upregulation of CXCL5 英文参考文献.doc

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Defects in Actin Dynamics Lead to an Autoinflammatory Condition through the Upregulation of CXCL5 英文参考文献

DefectsinActinDynamicsLeadtoanAutoinflammatory ConditionthroughtheUpregulationofCXCL5 AngelaM.Verdoni1,RichardS.Smith2,AkihiroIkeda1*,SakaeIkeda1* 1DepartmentofMedicalGenetics,UniversityofWisconsin-Madison,Madison,Wisconsin,UnitedStatesofAmerica,2TheJacksonLaboratory,BarHarbor,Maine,United StatesofAmerica Abstract Background: Destrin (DSTN) is a member of the ADF/cofilin family of proteins and is an important regulator of actin dynamics. The primary function of destrin is to depolymerize filamentous actin into its monomeric form and promote filamentsevering.WhileprogresshasbeenmadeinunderstandingthebiochemicalfunctionsoftheADF/cofilinproteins, thestudyofananimalmodelforcellsdeficientforDSTNprovidesanopportunitytoinvestigatethephysiologicalprocesses regulatedbyproperactindynamicsinvivo.Aspontaneousmousemutant,cornealdisease1(corn1),isdeficientforDSTN, whichcausesepithelialhyperproliferationandneovascularizationinthecornea. Dstncorn1 miceexhibitanactindynamics defectinthecorneaasevidencedbytheformationofactinstressfibersintheepithelialcells.Previously,weobserveda significant infiltration of leukocytes into the cornea of Dstncorn1 mice as well as the upregulation of proinflammatory molecules.Inthisstudy,wesoughttocharacterizethisinflammatoryconditionandexplorethephysiologicalmechanism throughwhichalossofDstnfunctionleadstoinflammation. Methodology/Principal Findings: Through immunofluorescent analyses, we observed a significant recruitment of neutrophils and macrophages to the Dstncorn1 cornea, demonstrating that the innate immune system is spontaneously activatedinthismutant.Theinflammatorychemokine,CXCL5,wasectopicallyexpressedinthecornealepithelialcellsof Dstncorn1mice,andtargetingofthereceptorforthischemokineinhibitedneutrophilrecruitment.Aninflammatoryreaction was not observed in the cornea of allelic mutant strain, Dstncorn1-2J, which has a milder defect in actin dynamics in the cornealepithelialcells. Conclusions/Significance:Thisstudyshowsthatseveredefects