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dc.contributor.authorYang, YH
dc.contributor.authorHamilton, JA
dc.date.available2014-05-21T19:30:29Z
dc.date.issued2001-01-01
dc.identifierhttp://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000166659100015&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=d4d813f4571fa7d6246bdc0dfeca3a1c
dc.identifier.citationYang, Y. H. & Hamilton, J. A. (2001). Dependence of interleukin-1-induced arthritis on granulocyte-macrophage colony-stimulating factor. ARTHRITIS AND RHEUMATISM, 44 (1), pp.111-119. https://doi.org/10.1002/1529-0131(200101)44:1<111::AID-ANR15>3.0.CO;2-1.
dc.identifier.issn0004-3591
dc.identifier.urihttp://hdl.handle.net/11343/26384
dc.descriptionC1 - Journal Articles Refereed
dc.description.abstractOBJECTIVE: To determine whether granulocyte-macrophage colony-stimulating factor (GM-CSF) and macrophage CSF (M-CSF or CSF-1) are involved in the methylated bovine serum albumin/interleukin-1 (mBSA/IL-1)-induced arthritis model. METHODS: Following systemic injection, IL-1 has been shown to augment a weak inflammatory response to mBSA in murine joints and to induce an acute erosive arthritis. GM-CSF and M-CSF have been implicated in inflammatory reactions, including those in joints, and have recently been shown to exacerbate murine arthritis. Since in vitro studies have found that IL-1 can enhance GM-CSF and M-CSF production, we reasoned that they might be playing a part in IL-1-mediated arthritis. GM-CSF-deficient (GM-CSF-/-) and M-CSF-deficient (op/op) mice were injected intraarticularly with mBSA and subcutaneously with IL-1. Arthritis was monitored histologically on day 7. Normal mice were also treated intraperitoneally with blocking monoclonal antibodies to GM-CSF and M-CSF, and to the M-CSF receptor. Numbers of macrophages (Mac-2 and F4/80 staining) were monitored, as was the number of cycling (bromodeoxyuridine-positive) cells. RESULTS: GM-CSF-/- mice and normal mice treated with anti-GM-CSF antibody did not show IL-1-induced arthritis progression. There was a dramatic reduction in synovial cellularity, including reduced numbers of macrophages and cycling cells. The op/op mice did not develop mBSA/IL-1-induced disease, but blocking antibody to M-CSF or to the M-CSF receptor failed to diminish disease in normal mice. CONCLUSION: GM-CSF is involved in the IL-1-induced arthritis that follows mBSA injection; M-CSF involvement in the model is also suggested, since op/op mice did not develop arthritis. These studies provide the first in vivo evidence for a role of GM-CSF, and possibly M-CSF, in the proinflammatory actions of IL-1.
dc.formatapplication/pdf
dc.languageEnglish
dc.publisherLIPPINCOTT WILLIAMS & WILKINS
dc.subjectRheumatology and Arthritis ; Skeletal System and Disorders (incl. Arthritis)
dc.titleDependence of interleukin-1-induced arthritis on granulocyte-macrophage colony-stimulating factor
dc.typeJournal Article
dc.identifier.doi10.1002/1529-0131(200101)44:1<111::AID-ANR15>3.0.CO;2-1
melbourne.peerreviewPeer Reviewed
melbourne.affiliationThe University of Melbourne
melbourne.affiliation.departmentMedicine - Royal Melbourne And Western Hospitals
melbourne.source.titleARTHRITIS AND RHEUMATISM
melbourne.source.volume44
melbourne.source.issue1
melbourne.source.pages111-119
dc.research.coderfcd321028
dc.research.codeseo1998730114
melbourne.publicationid438
melbourne.elementsid246565
melbourne.contributor.authorHamilton, John
melbourne.contributor.authorYANG, YUANHANG
dc.identifier.eissn1529-0131
melbourne.accessrightsThis item is currently not available from this repository


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