Neutrophils mediate edema formation but not mechanical allodynia during zymosan‐induced inflammation

Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society

关键词: pain;    nociceptor;    platelets;    von Willebrand factor;    GPIbα;   

DOI  :  10.1189/jlb.3A1213-628R

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

Inflammatorypainisbasedonstimulationandsensitizationofperipheralendingsofsensoryneurons(nociceptors)bypronociceptivemediators.Thesemediatorscanbereleasedbyresidentcells,aswellasinvadingimmunecells.Althoughneutrophilsareknowntoreleasevariousmediators,whichcanstimulateorsensitizenociceptors,theextentoftheircontributiontonociceptiveresponsesisunclear.Here,westudiedthecontributionofneutrophilstozymosan‐inducedinflammatorypain,whichischaracterizedbyanearlyrecruitmentofhighnumbersofneutrophils.Surprisingly,antibody‐mediatedneutrophildepletioncausedacompletelossofedemaformationbuthadnoeffectonmechanicalpainthresholds.BlockageoftheinteractionbetweenneutrophilsandplateletsorendothelialcellsusingantibodiesdirectedagainstCD11bandCD162reducedneutrophilrecruitmenttothesiteofinflammation.Again,thetreatmentdecreasedzymosan‐inducededemaswithoutalteringmechanicalpainthresholds.Also,HLB‐219mice,whichhavefiveto10timeslessplateletsthanWTmice,showedreducedneutrophilrecruitmenttothesiteofinflammationanddecreasededemasizes,whereas,again,mechanicalthresholdswereunaltered.TheeffectsobservedinHLB‐219micewererelativelysmallandnotreproducedinvWF‐deficientmiceorafterantibody‐mediatedblockageofGPIbα.Flowchamberandtransmigrationassaysshowedthatplateletswerenotnecessaryforneutrophiladhesiontoendothelialcellsbutincreasedtheirtransmigration.Takentogether,zymosan‐inducedmechanicalallodyniais,incontrasttoedemaformation,independentofneutrophils,andrecruitmentofneutrophilsisonlypartlyinfluencedbyinteractionswithplatelets...

【 授权许可】

CC BY