Regulation of the Formyl Peptide Receptor 1 (FPR1) Gene in Primary Human Macrophages 英文参考文献.docVIP
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Regulation of the Formyl Peptide Receptor 1 (FPR1) Gene in Primary Human Macrophages 英文参考文献
RegulationoftheFormylPeptideReceptor1(FPR1)
GeneinPrimaryHumanMacrophages
ClaudioGemperle1,2,3.,MattiaSchmid1,2,3.,MagdalenaHerova1,2,3,JacquelineMarti-Jaun1,2,3
SophiaJ.A.Wuest1,2,3,ChristaLoretz1,2,3,MartinHersberger1,2,3
,
*
1DivisionofClinicalChemistryandBiochemistry,UniversityChildren’sHospitalZurich,Zurich,Switzerland, 2Children’sResearchCenter,UniversityChildren’sHospital
Zurich,Zurich,Switzerland,3CenterforIntegrativeHumanPhysiology,UniversityofZurich,Zurich,Switzerland
Abstract
The formyl peptide receptor 1 (FPR1) is mainly expressed by mammalian phagocytic leukocytes and plays a role in
chemotaxis,killingofmicroorganismsthroughphagocytosis,andthegenerationofreactiveoxygenspecies.Alargenumber
of ligands have been identified triggering FPR1 including formylated and non-formylated peptides of microbial and
endogenous origin. While the expression of FPR1 in neutrophils has been investigated intensively, knowledge on the
regulationofFPR1expressioninpolarizedmacrophagesislacking.Inthisstudyweshowthatprimaryhumanneutrophils,
monocytesandrestingmacrophagesdoexpressthereceptorontheircellsurface.PolarizationofmacrophageswithIFNc,
LPS and with the TLR8 ligand 3M-002 further increases FPR1 mRNA levels but does not consistently increase protein
expressionorchemotaxistowardstheFPR1ligandfMLF.Incontrast,polarizationofprimaryhumanmacrophageswithIL-4
andIL-13leadingtothealternativeactivatedmacrophages,reducesFPR1cellsurfaceexpressionandabolisheschemotaxis
towardsfMLF.TheseresultsshowthatM2macrophageswillnotreacttotriggeringofFPR1,limitingtheroleforFPR1to
chemotaxisandsuperoxideproductionofrestingandpro-inflammatoryM1macrophages.
Citation:GemperleC,SchmidM,HerovaM,Marti-JaunJ,WuestSJA,etal.(2012)RegulationoftheFormylPeptideReceptor1(FPR1)GeneinPrimaryHuman
Macrophages.PLoSONE7(11):e50195.doi:10.1371/journal.pone.0050195
Editor:Jo¨rnCoers,DukeUniversityMedicalCenter,UnitedStatesofAmerica
ReceivedJuly26,2012;AcceptedOctober18,2012;PublishedNovember21,2012
Copyright: ?
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