Focused Examination of the Intestinal lamina Propria Yields Greater Molecular Insight into Mechanisms Underlying SIV Induced Immune Dysfunction 英文参考文献.docVIP

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Focused Examination of the Intestinal lamina Propria Yields Greater Molecular Insight into Mechanisms Underlying SIV Induced Immune Dysfunction 英文参考文献.doc

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Focused Examination of the Intestinal lamina Propria Yields Greater Molecular Insight into Mechanisms Underlying SIV Induced Immune Dysfunction 英文参考文献

FocusedExaminationoftheIntestinallaminaPropria YieldsGreaterMolecularInsightintoMechanisms UnderlyingSIVInducedImmuneDysfunction MaheshMohan1,DeepakKaushal2,PyoneP.Aye1,XavierAlvarez1,RonaldS.Veazey1, AndrewA.Lackner1* 1Division of Comparative Pathology, Tulane National Primate Research Center, Covington, Louisiana, United States of America, 2Division of Bacteriology and Parasitology,TulaneNationalPrimateResearchCenter,Covington,Louisiana,UnitedStatesofAmerica Abstract Background:TheGastrointestinal(GI)tractiscriticaltoAIDSpathogenesisasitistheprimarysiteforviraltransmissionand a major site of viral replication and CD4 T cell destruction. Consequently GI disease, a major complication of HIV/SIV + infectioncanfacilitatetranslocationoflumenalbacterialproductscausinglocalized/systemicimmuneactivationleadingto AIDSprogression. Methodology/Principal Findings: To better understand the molecular mechanisms underlying GI disease we analyzed global gene expression profiles sequentially in the intestine of the same animals prior to and at 21 and 90d post SIV infection (PI). More importantly we maximized information gathering by examining distinct mucosal components (intraepithelial lymphocytes,laminaproprialeukocytes[LPL],epitheliumandfibrovascular stroma)separately. Theuseof sequential intestinal resections combined with focused examination of distinct mucosal compartments represents novel approaches not previously attempted. Here we report data pertaining to the LPL. A significant increase (61.7-fold) in immunedefense/inflammation,celladhesion/migration,cellsignaling,transcriptionandcelldivision/differentiationgenes wereobservedat21and90dPI.GenesassociatedwiththeJAK-STATpathway(IL21,IL12R,STAT5A,IL10,SOCS1)andT-cell activation(NFATc1,CDK6,Gelsolin,Moesin)werenotablyupregulatedat21dPI.Markedlydownregulatedgenesat21dPI included IL17D/IL27 and IL28B/IFNc3 (anti-HIV/viral), activation induced cytidine deaminase (B-cell function) and approximately 57 genes regulating oxida