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dc.contributor.authorP. Sester, David
dc.contributor.authorTrieu, Angela
dc.contributor.authorBrion, Kristian
dc.contributor.authorSchroder, Kate
dc.contributor.authorRavasi, Timothy
dc.contributor.authorA. Robinson, Jodie
dc.contributor.authorMcDonald, Rebecca C.
dc.contributor.authorRipolla, Vera
dc.contributor.authorSuzuki, Harukazu
dc.contributor.authorHayashizaki, Yoshihide
dc.contributor.authorJ. Stacey, Katryn
dc.contributor.authorA. Hume, David
dc.contributor.authorSweet, Matthew J.
dc.contributor.authorA. Wells, Christine
dc.date.accessioned2017-05-03T15:01:04Z
dc.date.available2017-05-03T15:01:04Z
dc.date.issued2005
dc.date.modified2008-12-18T06:55:10Z
dc.identifier.issn01712985
dc.identifier.doi10.1016/j.imbio.2005.05.004
dc.identifier.urihttp://hdl.handle.net/10072/20921
dc.description.abstractWe previously reported that bacterial products such as LPS and CpG DNA down-modulated cell surface levels of the Colony Stimulating Factor (CSF)-1 receptor (CSF-1R) on primary murine macrophages in an all-or-nothing manner. Here we show that the ability of bacterial products to down-modulate the CSF-1R rendered bone marrow-derived macrophages (BMM) unresponsive to CSF-1 as assessed by Akt and ERK1/2 phosphorylation. Using toll-like receptor (tlr)9 as a model CSF-1-repressed gene, we show that LPS induced tlr9 expression in BMM only when CSF-1 was present, suggesting that LPS relieves CSF-1-mediated inhibition to induce gene expression. Using cDNA microarrays, we identified a cluster of similarly CSF-1 repressed genes in BMM. By real time PCR we confirmed that the expression of a selection of these genes, including integral membrane protein 2B (itm2b), receptor activity-modifying protein 2 (ramp2) and macrophage-specific gene 1 (mpg-1), were repressed by CSF-1 and were induced by LPS only in the presence of CSF-1. This pattern of gene regulation was also apparent in thioglycollate-elicited peritoneal macrophages (TEPM). LPS also counteracted CSF-1 action to induce mRNA expression of a number of transcription factors including interferon consensus sequence binding protein 1 (Icsbp1), suggesting that this mechanism leads to transcriptional reprogramming in macrophages. Since the majority of in vitro studies on macrophage biology do not include CSF-1, these genes represent a set of previously uncharacterised LPS-inducible genes. This study identifies a new mechanism of macrophage activation, in which LPS (and other toll-like receptor agonists) regulate gene expression by switching off the CSF-1R signal. This finding also provides a biological relevance to the well-documented ability of macrophage activators to down-modulate surface expression of the CSF-1R.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherGustav Fischer Verlag
dc.publisher.placeGermany
dc.publisher.urihttp://www.elsevier.com/wps/find/journaldescription.cws_home/701769/description#description
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrom97
dc.relation.ispartofpageto107
dc.relation.ispartofissue2-4
dc.relation.ispartofjournalImmunobiology
dc.relation.ispartofvolume210
dc.rights.retentionN
dc.subject.fieldofresearchBiological Sciences
dc.subject.fieldofresearchAgricultural and Veterinary Sciences
dc.subject.fieldofresearchMedical and Health Sciences
dc.subject.fieldofresearchcode06
dc.subject.fieldofresearchcode07
dc.subject.fieldofresearchcode11
dc.titleLPS regulates a set of genes in primary murine macrophages by antagonising CSF-1 action
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.date.issued2005
gro.hasfulltextNo Full Text
gro.griffith.authorWells, Christine


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