Alveolar Epithelial Type II Cells Activate Alveolar Macrophages and Mitigate P. Aeruginosa Infection 英文参考文献.docVIP
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Alveolar Epithelial Type II Cells Activate Alveolar Macrophages and Mitigate P. Aeruginosa Infection 英文参考文献
AlveolarEpithelialTypeIICellsActivateAlveolar
MacrophagesandMitigateP.AeruginosaInfection
ShibichakravarthyKannan1,HuangHuang1,DrewSeeger1,AaronAudet1,YaoyuChen2 ,Canhua
Huang3,HongweiGao1,ShaoguangLi2,MinWu1,3*
1Department of Biochemistry and Molecular Biology, University of North Dakota, Grand Forks, North Dakota, United States of America, 2Division of Hematology/
Oncology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, United States of America, 3State Key Laboratory for
Biotherapy,WestChinaHospital,SichuanUniversity,Chengdu,China
Abstract
AlthoughalveolarepithelialtypeIIcells(AECII)performsubstantialrolesinthemaintenanceofalveolarintegrity,theextent
of their contributions to immune defense is poorly understood. Here, we demonstrate that AECII activates alveolar
macrophages(AM)functions,suchasphagocytosisusingaconditionedmediumfromAECIIinfectedbyP.aeruginosa .AECII-
derivedchemokineMCP-1,amonocytechemoattractantprotein,wasidentifiedasamainfactorinenhancingAMfunction.
WeproposedthattheenhancedimmunepotencyofAECIImayplayacriticalroleinalleviationofbacterialpropagationand
pneumonia. The ability of phagocytosis and superoxide release by AM was reduced by MCP-1 neutralizing antibodies.
Furthermore,MCP-12/2miceshowedanincreasedbacterialburdenunderPAO1andPAKinfectionvs.wtlittermates.AM
from MCP-12/2 mice also demonstrated less superoxide and impaired phagocytosis over the controls. Inaddition, AECII
conditioned medium increased the host defense of airway in MCP-12/2 mice through the activation of AM function.
Mechanistically, we found that Lyn mediated NFkB activation led to increased gene expression and secretion of MCP-1.
ConsequentlyLyn2/2micehadreducedMCP-1secretionandresultedinadecreaseinsuperoxideandphagocytosisbyAM.
Collectively,ourdataindicatethatAECIImayserveasanimmuneboosterforfightingbacterialinfections,particularlyin
severeimmunocompromisedconditions.
Citation:KannanS,HuangH,SeegerD,AudetA,ChenY,etal.(2009)Alveol
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