Fig. 6.

Absence of NK cells is associated with reduced poststroke inflammatory response in the brain. (A) Absence of NK cells reduces brain inflammation during stroke. Brain homogenates were prepared from mice of the indicated groups 12, 24, 72, and 96 h after MCAO. Cytokine concentrations were measured by a Multi-Analyte ELISArray Kit (SABiosciences). Results shown are from three independent experiments with a pool of n = 4 mice per group per time point. *P < 0.05, **P < 0.01, Rag2^−/−γc^−/− vs. Rag2^−/−; ^#P < 0.05, ^##P < 0.01, Cx3cr1^+/+ NK→Rag2^−/−γc^−/− vs. Cx3cr1^−/− NK→Rag2^−/−γc^−/−. (B–E) Lack of NK cells is associated with reduced expression of inflammatory mediators in the ischemic brain. Representative images of immunostaining for IL-1β and IL-6 from brain sections of an infarct hemisphere from mice with (Rag2^−/−) or without (Rag2^−/−γc^−/−) NK cells (B and D) and quantification of cytokines (C and E) at 24 h after the MCAO procedure by ELISA. (Scale bars, 20 µm.) n = 8 per group. **P < 0.01. (F and G) Lack of NK cells reduced ROS generation in stroke. (F) Imaging ROS activity in vivo. Bioluminescent images were captured for 1 min using the cooled IVIS imaging system (Xenogen IVIS-200) after luminol i.p. injection, as recently described (16, 23, 33), to monitor the ROS generation in Rag2^−/− and Rag2^−/−γc^−/− MCAO brains. (G) Quantification and statistical analysis of the images. Rag2^−/− and Rag2^−/−γc^−/− mice had significant differences in ROS levels after MCAO. Data were generated 12 h after MCAO, with seven mice per group. **P < 0.01.