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Higher expression of XO and lower activity of SOD1 in IAV-infected Prnp0/0 lungs.

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posted on 03.05.2018, 17:51 authored by Junji Chida, Hideyuki Hara, Masashi Yano, Keiji Uchiyama, Nandita Rani Das, Etsuhisa Takahashi, Hironori Miyata, Yukiko Tomioka, Toshihiro Ito, Hiroshi Kido, Suehiro Sakaguchi

(A) Western blotting of the lungs of WT and Prnp0/0 mice uninfected (Un) and infected with IAV/PR8 (100 IFU) at 5 dpi for XO. Actb is an internal control. Right panel: Quantification of XO after normalization against β-actin. Signal intensity of XO in lungs was evaluated against that in uninfected WT lungs. (B) Mortality and body weight of allopurinol-treated WT (n = 24) and Prnp0/0 (n = 11) mice and of control PBS-treated WT (n = 11) and Prnp0/0 (n = 10) mice after intranasal infection with 100 IFU of IAV/PR8. The p value for mortality: PBS-treated vs allopurinol-treated WT mice, p = 0.0104; PBS-treated vs allopurinol-treated Prnp0/0 mice, p = 0.0005; PBS-treated WT vs Prnp0/0 mice, p<0.0001; allopurinol-treated WT vs Prnp0/0 mice, p = 0.0529. Right panel: Viral titers in the lungs of each group of mice uninfected (Un) or infected with IAV/PR8 (100 IFU) at 3, 5, and 8 dpi (n = 3 in each mouse group). (C) Western blotting of the lungs of WT and Prnp0/0 mice uninfected and infected with IAV/PR8 (100 IFU) at 5 dpi for SOD1 and 2. Actb is an internal control. (D) SOD activity in the lungs of WT, Prnp0/0, and Tg(PrPΔOR)/Prnp0/0 mice uninfected and infected with IAV/PR8 (100 IFU) after treatment with or without DDC (n = 3 for each mouse group). (E) Cu ion content in uninfected WT, Prnp0/0, and Tg(PrPΔOR)/Prnp0/0 lungs (n = 3 for each mouse group). The 0 dpi in the graphs of survival rate and body weight is 5–10 min after infection. Un, uninfected. **, p<0.01; NS, not significant. Error bars, SD.

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