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1、Jpn.J.Infect.Dis.,69,405–413,2016OriginalArticleContributionofLewisXCarbohydrateStructuretoNeuropathogenicMurineCoronaviralSpreadMasatoshiKakizaki1,AkiraTogayachi2,HisashiNarimatsu2,andRihitoWatanabe1*1DepartmentofBioinformatics,GraduateSchoolofEngineering,SokaUniversity,T
2、okyo192-8577;and2GlycoscienceandGlycotechnologyResearchGroup,BiotechnologyResearchInstituteforDrugDiscovery,NationalInstituteofAdvancedIndustrialScienceandTechnology(AIST),Ibaraki305-8568,JapanSUMMARY:AlthoughLewisX(Lex),acarbohydratestructure,isinvolvedininnateimmunitythr
3、oughcell-to-cellandpathogenrecognition,itsexpressionhasnotbeenobservedinmousemonocytes/macrophages(Mo/Mas).TheMo/Masthatinfiltratethemeningesafterinfectionwiththeneuropathogenicmurinecoronavirusstrainsrr7areaninitialtargetofinfection.Furthermore,higherinflammatoryresponses
4、wereobservedingene-manipulatedmicelackinga1,3-fucosyltransferase9,whichdeterminestheexpressionoftheLexstructure,thaninwildtypemiceafterinfection.Weinves-tigatedLexexpressionusingCD11b-positiveperitonealexudatecells(PECs)andfoundthatLexisin-ducibleinMo/Masafterinfectionwith
5、srr7,especiallyinthesyncytialcellsduringthelatephaseofinfection.ThenumberofsyncytialcellswasreducedaftertreatmentoftheinfectedPECswithanti-Lexantibody,duringthelatephaseofinfection.Inaddition,theantibodytreatmentinducedamarkedreductioninthenumberoftheinfectedcellsat24hours
6、postinoculation,withoutchangingtheinfectedcellnumbersduringtheinitialphaseofinfection.ThesedataindicatethattheLexstructurecouldplayaroleinsyncytialformationandcell-to-cellinfectionduringthelatephaseofinfection.MasareoftenfoundinthemeningesandventricularINTRODUCTIONcavity(5
7、).cl-2virus(cl-2),isolatedfromaneuropathogenicmu-Theneuropathologicallesionsinthebrain,includingrinecoronavirusmousehepatitisvirus(MHV)strain,demyelination(7,8),inducedbyJHMinfectionarecon-JHMvirus(JHM)(1),exhibitsextremelyhighneu-sideredtobe,tosomeextent,theresultsofanind
8、irectrovirulenceafterinfection,leadinginfectedmicetomechanismofinfection.srr7inducesspong
