Reciprocal Interaction between Macrophages and T cells Stimulates IFN-γ and MCP-1 Production in Ang II-induced Cardiac Inflammation and Fibrosis 英文参考文献.docVIP

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Reciprocal Interaction between Macrophages and T cells Stimulates IFN-γ and MCP-1 Production in Ang II-induced Cardiac Inflammation and Fibrosis 英文参考文献.doc

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Reciprocal Interaction between Macrophages and T cells Stimulates IFN-γ and MCP-1 Production in Ang II-induced Cardiac Inflammation and Fibrosis 英文参考文献

ReciprocalInteractionbetweenMacrophagesandTcells StimulatesIFN-candMCP-1ProductioninAngII-induced CardiacInflammationandFibrosis Ya-leiHan1,Yu-linLi1,Li-xinJia1,Ji-zhongCheng1,Yong-fenQi1,2,Hong-jiaZhang1,2,JieDu1,2 * 1BeijingAnZhenHospital,CapitalMedicalUniversity,Beijing,China,2TheKeyLaboratoryofRemodeling-relatedCardiovascularDiseases,MinistryofEducation,Institute ofHeartLungandBloodVesselDiseases,Beijing,China Abstract Background: The inflammatory response plays a critical role in hypertension-induced cardiac remodeling. We aimed to study how interaction among inflammatory cells causes inflammatory responses in the process of hypertensive cardiac fibrosis. Methodology/PrincipalFindings:InfusionofangiotensinII(AngII,1500ng/kg/min)inmicerapidlyinducedtheexpression ofinterferonc(IFN-c)andleukocytesinfiltrationintotheheart.TodeterminetheroleofIFN-concardiacinflammationand remodeling,bothwild-type(WT)andIFN-c-knockout(KO)micewereinfusedAngIIfor7days,andwerefoundanequal bloodpressureincrease.However,knockoutofIFN-cpreventedAngII-induced:1)infiltrationofmacrophagesandTcells intocardiactissue;2)expressionoftumornecrosisfactoraandmonocytechemoattractantprotein1(MCP-1),and3)cardiac fibrosis, including the expressionof a-smooth muscle actin andcollagen I(all p,0.05). Cultured T cells or macrophages alone expressed very low level of IFN-c, however, co-culture of T cells and macrophages increased IFN-c expression by 19.860.95folds(vs.WTmacrophage,p,0.001)and20.962.09folds(vs.WTTcells,p,0.001).Invitroco-culturestudies using T cells and macrophages from WT or IFN-c KO mice demonstrated that T cells were primary source for IFN-c production.Co-cultureofWTmacrophageswithWTTcells,butnotwithIFN-c-knockoutTcells,increasedIFN-cproduction (p,0.01). Moreover, IFN-c produced by T cells amplified MCP-1 expression in macrophages andstimulated macrophage migration. Conclusions/Significance: Reciprocal interaction between macrophages and T cells in heart stimulates IFN-c expression, lead