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Interleukin-10 Inhibits Macrophage-Induced Glomerular Injury

Centre for Inflammatory Diseases, Monash University Department of Medicine, Clayton, Victoria, Australia.

Correspondence to Dr. Peter G. Tipping, Centre for Inflammatory Diseases, Monash University Department of Medicine, Level 5, Block E, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia. Phone: +61 3 9594 5547; Fax: +61 3 9594 4279; E-mail: peter.tipping{at}med.monash.edu.au

The ability of interleukin-10 (IL-10) to inhibit macrophage recruitment, activation, and proliferation in vivo was studied in a macrophage-mediated, but T cell-independent, passive anti-glomerular basement membrane antibody-induced model of glomerulonephritis (GN) in rats. Treatment with recombinant murine IL-10 resulted in dose-dependent reductions in proteinuria (high dose: 16 ± 1 mg/24 h; low dose: 30 ± 2 mg/24 h; control treatment: 69 ± 6 mg/24 h; normal: 7 ± 1 mg/24 h) and glomerular macrophage recruitment (high dose: 1.8 ± 0.1 macrophages per glomerular cross section [c/gcs]; low dose: 5.5 ± 0.2 c/gcs; control treatment: 12.1 ± 0.6 c/gcs). Macrophage and intrinsic glomerular cell proliferation were reduced at both doses of IL-10, as was glomerular expression of P-selectin and monocyte chemoattractant protein-1. IL-10 treatment also resulted in a dose-dependent reduction of macrophage activation as indicated by MHC class II and IL-1ß expression. Glomerular nitrite production by isolated cultured glomeruli was reduced after IL-10 treatment in vivo (high dose: 2.3 ± 2.3 nmol/10⁴ glomeruli per 72 h; low dose: 28 ± 5 nmol/10⁴ glomeruli per 72 h; control treatment: 82 ± 11 nmol/10⁴ glomeruli per 72 h). Tumor necrosis factor- production was abolished by high-dose treatment and reduced by the lower dose (3.8 ± 3.8 pg/10⁴ glomeruli per 72 h; control treatment: 249 ± 23 pg/10⁴ glomeruli per 72 h). These studies demonstrate that IL-10 directly attenuates glomerular macrophage recruitment, activation, and proliferation in vivo and can significantly attenuate macrophage-mediated GN independent of any effects on T cells.

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