Figure 3.
Neutrophilic infiltration to the renal parenchyma after injury is IL-6 dependent and promotes renal injury. (A) Few peritubular neutrophils are present at baseline in IL-6+/+ mice. Accumulation of neutrophils in peritubular capillaries at the inner cortex and outer medulla accompanied by neutrophilic extravasation into the renal interstitium is evident 24 h after HgCl2 administration. Peritubular accumulation of neutrophils in IL-6−/− mice after HgCl2 administration was significantly diminished compared with IL-6+/+ mice but not significantly different than in naïve IL-6+/+ mice. Quantification of renal neutrophilic infiltration in IL-6+/+ and IL-6−/− mice 24 h after HgCl2 administration is shown. Data are means ± SEM. *P ≅ 0.04 (n = 7) versus other groups. (B) Macrophage infiltration after AKI is not IL-6 dependent. Staining and quantification of renal macrophages in the inner cortex in IL-6+/+ and IL-6−/− mice 24 h after HgCl2 administration. Data are mean ± SEM. *P < 0.05 (n = 7) versus other groups. (C) Effect of neutrophil depletion on HgCl2-induced AKI. BUN levels in antineutrophil serum (□), control serum (▪), and untreated (baseline; □) are shown. Data are means ± SEM. *P ≅ 0.003 and ≅ 0.01 versus control serum + HgCl2–treated and untreated mice, respectively. HPF, high-power field. Magnification, ×200.