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. Author manuscript; available in PMC: 2017 Sep 8.
Published in final edited form as: Cell. 2016 Sep 8;166(6):1512–1525.e12. doi: 10.1016/j.cell.2016.07.026

Figure 5. Inhibition of glucose utilization in Poly(I:C)-induced inflammation enhances ER stress.

Figure 5

(A) B6 WT and Ifnar-/- mice were challenged with Poly(I:C), then treated with either IP PBS or 2DG. Whole hindbrain lysates 24 hours after Poly(I:C) treatment immunoblotted for CHOP and β-Tubulin.

(B) Hindbrain mRNA expression of Gadd34 18 hours after Poly(I:C) challenge and treatment with IP PBS, glucose, or 2DG in WT mice. n=5/group (one death in Poly(I:C) group).

(C) Survival of B6 WT mice and Ddit3-/- mice after Poly(I:C) challenge and treatment with IP PBS or 2DG. WT vs Ddit3-/- p=0.0015 WT: Poly(I:C) + 2DG vs Ddit3-/-: Poly(I:C) + 2DG, n=5/group.

(D and E) B6 WT and Ddit3-/- mice were challenged with Poly(I:C) and treated with 2DG.

(D) Plasma IFNα after Poly(I:C) challenge and treatment with 2DG. n=5/group.

(E) Vital signs measured 18 hours after Poly(I:C) + 2DG. n=3-7/group (vital sign values of B6 WT mice same as those in Figure 4D)

(F-H) B6 WT mice and Ddit3-/- mice were infected with 700 PFU of influenza virus and treated with 2DG.

(F) Survival after influenza infection and treatment with 2DG. p=0.048 n=5/group (G) Plasma IFNα after influenza infection and treatment with 2DG. n=5/group.

(H) Lung and BAL viral load 5 days post-infection. n=5/group.

Data are represented as mean ± SEM. **p<0.01, ***p<0.001. See also Figure S5.