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Macrophage accumulation at a site of renal inflammation is dependent on the M‐CSF/c‐fms pathway
Author(s) -
Le Meur Yannick,
Tesch Gregory H.,
Hill Prudence A.,
Mu Wei,
Foti Rita,
NikolicPaterson David J.,
Atkins Robert C.
Publication year - 2002
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.72.3.530
Subject(s) - macrophage , inflammation , monocyte , macrophage colony stimulating factor , biology , kidney , receptor , medicine , endocrinology , immunology , biochemistry , in vitro
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.