Figure 2.

B1R deficiency or blockade ameliorates induction of murine MPO-ANCA GN. WT B6 (n=7) mice, B1R^−/− mice (n=9), and mice that were pretreated with vehicle (PBS) (n=5) or specific B1R antagonist (n=5) were intravenously injected with anti-MPO IgG (50 µg/g body wt). Mice were euthanized on day 6 after injection of anti-MPO. Severity of GN was measured by calculating the percentage of glomeruli with crescents and necrosis by counting all glomeruli in cross-sections of both kidneys. (A) Glomerular crescent formation and (B) necrosis induced by anti-MPO were absent or reduced in all B1R^−/− mice and B1R antagonist-treated mice compared with WT B6 and vehicle treated mice, respectively. (C) Urine hematuria (dipstick scale, 0–4+) was also reduced in B1R^−/− and B1R antagonist-treated mice. (D) Measurement by ELISA of circulating anti-MPO titers at euthanasia demonstrated similar levels in all groups after anti-MPO IgG injection.