Fig. 5.

Mtb infection upregulates STING/cGAS expression, but this pathway does not influence proinflammatory cytokine production in the lungs. The lungs of Mtb-infected mice (10³ CFU) were collected at 28 or 88 days postinfection (d28 or d88), and homogenized for RNA isolation or supernatant collection. a Expression of the STING coding gene Tmem173 and the cGAS coding gene Mb21d1 was evaluated by real-time qPCR during the infection in the WT mice. Statistically significant difference compared to day 28: * p < 0.05 (two-way ANOVA followed by the Bonferroni post hoc test). b Similarly, Ifn-β expression was determined in WT, STING^–/–, and cGAS^–/– mice. The fold change of mRNA levels was normalized to the Gapdh level in the uninfected WT mice. c–f Lung homogenates from infected WT, STING^–/–, cGAS^–/–, IFNAR^–/–, IFNGR1^–/–, and TNFα^–/– mice were analyzed for IFN-γ, IL-12p40, IL23p19, or CXCL10 production by ELISA. The IFNGR1^–/– and TNFα^–/– mice did not survive for 88 days. Data are shown as mean ± SD of n = 5 mice per group and the results presented are from 1 experiment representative of 3 independent experiments. Statistically significant difference in relation to WT: * p < 0.05; ** p < 0.01; *** p < 0.001 (two-way ANOVA followed by the Bonferroni post hoc test).