{"doi":"10.1189/jlb.72.3.530","title":"Macrophage accumulation at a site of renal inflammation is dependent on the M-CSF/c-fms pathway","abstract":"<jats:title>Abstract</jats:title><jats:p>Production of macrophage-colony stimulating factor (M-CSF), the major macrophage growth factor, is increased in tissues during inflammation. Therefore, w determined whether M-CSF, acting through its receptor c-fms, contributes to macrophage accumulation at a site of tissue injury. Daily treatment with anti-c-fms or control antibody was given to mice with renal inflammation resulting from unilateral ureteric obstruction (UUO). Following UUO, kidney M-CSF mRNA increased in association with macrophage accumulation (days 1, 5, and 10) and local macrophage proliferation (days 5 and 10). Anti-c-fms treatment caused a minor inhibition of monocyte recruitment at day 1, reduced macrophage accumulation by 75% at day 10, but did not affect blood monocyte counts or the CD4 and CD8 lymphocytic infiltrate. Prevention of macrophage accumulation by anti-c-fms treatment was associated with a 90% reduction in local macrophage proliferation at days 5 and 10 without evidence of increased macrophage apoptosis. Therefore, M-CSF/c-fms signaling plays a key role in macrophage accumulation during tissue injury.</jats:p>","journal":"Journal of Leukocyte Biology","year":2002,"id":688550,"datarank":0.6749714505495399,"base_score":4.499809670330265,"endowment":4.499809670330265,"self_citation_contribution":0.6749714505495399,"citation_network_contribution":0.0,"self_endowment_contribution":0.6749714505495399,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":89,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1798836,"name":"Gregory H Tesch","orcid":null,"position":1,"is_corresponding":false},{"id":1798837,"name":"Prudence A Hill","orcid":null,"position":2,"is_corresponding":false},{"id":576283,"name":"Wei Mu","orcid":"0000-0001-7970-8666","position":3,"is_corresponding":false},{"id":1798838,"name":"Rita Foti","orcid":null,"position":4,"is_corresponding":false},{"id":1798839,"name":"David J Nikolic-Paterson","orcid":null,"position":5,"is_corresponding":false},{"id":1798840,"name":"Robert C Atkins","orcid":null,"position":6,"is_corresponding":false},{"id":1798835,"name":"Yannick Le Meur","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Macrophage accumulation at a site of renal inflammation is dependent on the M-CSF/c-fms pathway","abstract":"<jats:title>Abstract</jats:title><jats:p>Production of macrophage-colony stimulating factor (M-CSF), the major macrophage growth factor, is increased in tissues during inflammation. Therefore, w determined whether M-CSF, acting through its receptor c-fms, contributes to macrophage accumulation at a site of tissue injury. Daily treatment with anti-c-fms or control antibody was given to mice with renal inflammation resulting from unilateral ureteric obstruction (UUO). Following UUO, kidney M-CSF mRNA increased in association with macrophage accumulation (days 1, 5, and 10) and local macrophage proliferation (days 5 and 10). Anti-c-fms treatment caused a minor inhibition of monocyte recruitment at day 1, reduced macrophage accumulation by 75% at day 10, but did not affect blood monocyte counts or the CD4 and CD8 lymphocytic infiltrate. Prevention of macrophage accumulation by anti-c-fms treatment was associated with a 90% reduction in local macrophage proliferation at days 5 and 10 without evidence of increased macrophage apoptosis. 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