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Pharmacological blockade of CCR1 ameliorates murine arthritis and alters cytokine networks in vivo
dc.contributor.authorAmat, M.en_US
dc.contributor.authorBenjamim, C. F.en_US
dc.contributor.authorWilliams, L. M.en_US
dc.contributor.authorPrats, N.en_US
dc.contributor.authorTerricabras, E.en_US
dc.contributor.authorBeleta, J.en_US
dc.contributor.authorKunkel, Steven Len_US
dc.contributor.authorGodessart, N.en_US
dc.date.accessioned2010-06-01T22:11:41Z
dc.date.available2010-06-01T22:11:41Z
dc.date.issued2006-11en_US
dc.identifier.citationAmat, M; Benjamim, C F; Williams, L M; Prats, N; Terricabras, E; Beleta, J; Kunkel, S L; Godessart, N (2006). "Pharmacological blockade of CCR1 ameliorates murine arthritis and alters cytokine networks in vivo ." British Journal of Pharmacology 149(6): 666-675. <http://hdl.handle.net/2027.42/75213>en_US
dc.identifier.issn0007-1188en_US
dc.identifier.issn1476-5381en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/75213
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=17016504&dopt=citationen_US
dc.description.abstractThe chemokine receptor CCR1 is a potential target for the treatment of rheumatoid arthritis. To explore the impact of CCR1 blockade in experimental arthritis and the underlying mechanisms, we used J-113863, a non-peptide antagonist of the mouse receptor. Experimental approach: Compound J-113863 was tested in collagen-induced arthritis (CIA) and three models of acute inflammation; Staphylococcus enterotoxin B (SEB)-induced interleukin-2 (IL-2), delayed-type hypersensitivity (DTH) response, and lipopolysaccharide (LPS)-induced tumour necrosis factorΑ (TNFΑ) production. In the LPS model, CCR1 knockout, adrenalectomised, or IL-10-depleted mice were also used. Production of TNFΑ by mouse macrophages and human synovial membrane samples in vitro were also studied. Key results: Treatment of arthritic mice with J-113863 improved paw inflammation and joint damage, and dramatically decreased cell infiltration into joints. The compound did not inhibit IL-2 or DTH, but reduced plasma TNFΑ levels in LPS-treated mice. Surprisingly, CCR1 knockout mice produced more TNFΑ than controls in response to LPS, and J-113863 decreased TNFΑ also in CCR1 null mice, indicating that its effect was unrelated to CCR1. Adrenalectomy or neutralisation of IL-10 did not prevent inhibition of TNFΑ production by J-113863. The compound did not inhibit mouse TNFΑ in vitro, but did induce a trend towards increased TNFΑ release in cells from synovial membranes of rheumatoid arthritis patients. Conclusions and implications: CCR1 blockade improves the development of CIA, probably via inhibition of inflammatory cell recruitment. However, results from both CCR1-deficient mice and human synovial membranes suggest that, in some experimental settings, blocking CCR1 could enhance TNF production. British Journal of Pharmacology (2006) 149 , 666–675. doi:en_US
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dc.publisherBlackwell Publishing Ltden_US
dc.rights2006 British Pharmacological Societyen_US
dc.subject.otherCCR1en_US
dc.subject.otherJ-113863en_US
dc.subject.otherChemokinesen_US
dc.subject.otherTNF Αen_US
dc.subject.otherIL-10en_US
dc.subject.otherCollagen-induced Arthritisen_US
dc.subject.otherInflammationen_US
dc.subject.otherRheumatoid Arthritisen_US
dc.titlePharmacological blockade of CCR1 ameliorates murine arthritis and alters cytokine networks in vivoen_US
dc.typeArticleen_US
dc.subject.hlbsecondlevelPharmacy and Pharmacologyen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationotherKennedy Institute of Rheumatology Division, Imperial College London, London, UKen_US
dc.identifier.pmid17016504en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/75213/1/sj.bjp.0706912.pdf
dc.identifier.doi10.1038/sj.bjp.0706912en_US
dc.identifier.sourceBritish Journal of Pharmacologyen_US
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dc.owningcollnameInterdisciplinary and Peer-Reviewed


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