Fig. 6: IL-1β mediates the macrophages inducing NETosis under poly(I:C) stimulation in vivo.
From: Hippo pathway and NLRP3-driven NETosis in macrophages: Mechanisms of viral pneumoniaaggravation
A Evaluation of IL-1β protein expression in macrophages isolated from the BALF of mice with poly(I:C) infection and treated with Hippo pathway inhibitors. B Quantitative analysis of the protein IL-1β relative to Tubulin under different conditions. C Measurement of Serum IL-1β level from mice with poly(I:C) infection and treated with Lats-IN-1 by ELISA. D NETosis biomarker levels from cells in the BALF of mice with poly(I:C) stimulation and neutralized IL-1β antibody were assessed by immunofluorescence. E Graphic presentations of fluorescence mean densities of CitH3 and MPO under different conditions. F CitH3 protein expression in the lung tissues from mice with poly(I:C) stimulation and neutralized IL-1β antibody was evaluated by western blotting. G Quantitative analysis of the protein CitH3 relative to Tubulin. H, I dsDNA and LL-37 levels in the BALF from mice infected with poly(I:C) and treated with neutralized IL-1β antibody, evaluated by ELISA. Note: IN, Lats-IN-1 is a potent and ATP-competitive inhibitor of LATS1 and LATS2 kinases. All data are representative as means ± s.e.m of three independent experiments. Student’s t test for (A–I); *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. Scale bar = 20 μm.
