北京白癜风主治医院哪里好 http://m.39.net/pf/bdfyy/bjzkbdfyy/Cross-talkbetweenthegutmicrobiotaandmonocyte-likemacrophagesmediatesaninflammatoryresponsetopromotecolitis-associatedtumourigenesis
YunbenYang,LiliLi,ChunjingXu,YunkeWang,ZhenWang,MengyaoChen,ZhouJiang,JunPan,ChenghuiYang,XiaoqianLi,KaiSong,JunfengYan,WanglanXie,XianguoWu,ZhigangChen,YingYuan,ShuZheng,JunYan,JianHuang,FumingQiu,
GutImmunol.(IF=19.)Pubdate:Nov19
DOI:10./gutjnl--
Abstract：
Objective
/p>
Macrophagesareamongthemostabundantcellsinthecolontumourmicroenvironment,andthereisacloserelationshipamongmonocytes,macrophagesandthegutmicrobiota.Alterationsinthegutmicrobiotaareinvolvedintumourdevelopment,buttheunderlyingmechanismsremainunclear.Weaimtoelucidatethetemporalchangesinmacrophagesubsetsandfunctions,andhowthesedynamicsareregulatedbymicrobialcuesintheinitiationofcolitis-associatedcancer.
Design/p>
Amousemodelofcolitis-associatedtumourigenesiswasestablishedtodeterminemacrophagedynamics.Theroleofmonocyte-likemacrophage(MLM)wasconfirmedbytargetingitschemotaxis.Theeffectsofthegutmicrobiotawereassessedbyantibiotictreatmentandfaecalmicrobiotatransplantation.
Results/p>
AselectiveincreaseinMLMswasobservedintheinitialstagesofcolitis-associatedcancer,withanenhancedsecretionofinflammatorycytokines.MLMaccumulationwasregulatedbyCCL2expressionofcolonicepithelialcells,whichwasinfluencedbybacteria-derivedlipopolysaccharide(LPS).LPSfurtherstimulatedinterleukin1βproductionfromMLMs,inducinginterleukin-17-producingT-helpercellactivationtopromoteinflammation.Theseobservationswerealsosupportedbyalteredmicrobial
