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. Author manuscript; available in PMC: 2021 Apr 30.
Published in final edited form as: Cell. 2020 Apr 15;181(3):674–687.e13. doi: 10.1016/j.cell.2020.03.040

Figure 4. Caspase-6 Contributes to Host Protection against IAV Infection In Vivo.

Figure 4.

(A) Body weight of 6 to 8-week-old wild-type (WT) and Casp6−/− mice infected intranasally with 50 plaque forming units (PFUs) of influenza A virus (IAV).

(B) Survival of 6- to 8-week-old WT and Casp6−/− mice infected intranasally with 50 PFUs of IAV.

(C) Survival of 6- to 8-week-old littermate Casp6+/− and Casp6−/− mice infected intranasally with 125 PFUs of IAV.

(D) Immunohistochemistry staining of viral nucleoprotein (NP) in the lungs collected from WT and Casp6−/− mice at day 5 post-infection.

(E and F) Lung viral titers in WT and Casp6−/− mice infected with IAV for 3 days (E) or 7 days (F).

(G and H) IL-1β levels in the bronchoalveolar lavage fluid (BALF) from WT and Casp6−/− mice infected with IAV for 3 days (G) or 7 days (H).

(I) Quantification of the percentage of the lung lesioned in WT and Casp6−/− mice infected with IAV for 5 days.

(J) Microscopic analysis of Arg1+ cells in the lung tissue of WT and Casp6−/− mice infected with IAV for 7 days.

The original magnification is ×10 and ×40 as indicated. NS, not significant; *p < 0.05, **p < 0.01, and ***p < 0.001. Analysis was performed using the Student’s t test (E–I), two-way ANOVA (A), and log-rank test (B and C). Data are shown as mean ± SEM (A and E–I). Data are pooled from 4 independent experiments (A and B).

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