Fig. 8.
Interleukin (IL)-11 is critical for isoflurane postconditioning–mediated reduction in renal neutrophil infiltration after ischemia and reperfusion. (A) Representative photomicrographs of four to six experiments for immunohistochemistry (brown staining) for neutrophil infiltration (×200) from kidneys IL-11 receptor wild-type (IL-11R WT) mice, IL-11 receptor–deficient (IL-11R knockout [KO]) mice, and IL-11R WT mice pretreated with IL-11–neutralizing antibody and subjected to 30-min renal ischemia and 24-h reperfusion. Scale bars in all panels of A are 100 μm. (B) Quantifications of infiltrated neutrophils per ×200 field in the kidneys of mice after renal ischemia reperfusion (RIR). * P < 0.05 versus vehicle-treated pentobarbital-anesthetized mice subjected to RIR. Error bars represent 1 SD. IL-11R WT mice anesthetized with pentobarbital after renal ischemia showed heavy neutrophil infiltration. Isoflurane postconditioning significantly attenuated renal tubular neutrophil infiltration after RIR. IL-11 deficiency (IL-11R KO) or IL-11 neutralization attenuated these reductions in renal neutrophil infiltration with isoflurane postconditioning in mice.