Skip to main content
. Author manuscript; available in PMC: 2021 Mar 17.
Published in final edited form as: Immunity. 2020 Mar 11;52(3):475–486.e5. doi: 10.1016/j.immuni.2020.02.002

Fig. 4. cGAS-STING pathway impairs endothelial regeneration and recovery from inflammatory injury.

Fig. 4.

(A) Quantification of BrdU+ lung endothelial cell from WT and cGas−/− mice post CLP for 72 h, n = 5. (B) Lung transvascular albumin permeability in WT and cGAS−/− mice with/without CLP challenge, n = 5–7. (C) Representative H&E staining of lung tissue from three independent experiments (WT and cGas−/−) post CLP challenge (24 and 72 h). Red arrows indicate infiltrated immune cells. Scale bar, 200 m. Br indicates bronchia; and V, vessels. (D) Myeloperoxidase (MPO) activity in mouse lungs after CLP challenge, n = 5–7. (E) IFN-1β concentration in serum from LPS treated WT and cGas−/− mice (10 mg/kg, i.p, 6h), n = 5. (F) Quantification of BrdU+ lung endothelial cells from WT mice post-LPS exposure (10 mg/kg, i.p) with or without treatment of the STING agonist, CMA, (10 mg/kg, i.p, every 24h from 24h-72h post LPS challenge) for up to 72h post-LPS, n = 5. (G) Lung transvascular albumin permeability in LPS treated mice with or without CMA treatment, n = 5. Data are shown as mean ± SD. * P < 0.05, * * P < 0.01, two-tailed t-test. Please also see Figure S4.