Fig. 3

Effect of Rgs2 deficiency on LPS-induced lung inflammation. Wild type mice were exposed to aerosolized PBS (20 ml) or LPS from E. coli 0127:B8 (20 ml at 150 μg/ml) for 30 min. The lungs were harvested 3, 6 or 24 h after LPS challenge and fixed for later sectioning. Lung sections were stained with H&E. a Representative H&E stained sections of left lung are shown at ×10 magnification. b The H&E stained sections were manually scored where: 0 = no inflammation around airways, 1 = (minimal) < 10% inflammation around airways, 2 = (mild) 10–25, 3: (moderate) 25–50%, 4: (high) > 50%. Data (N = 6–7) are plotted as mean ± SE. Significance relative to PBS control was assessed by ANOVA with a Dunn’s post test. P ≤ 0.01 (**). c Morphometric analysis of ASM thickness. Data (N = 8) are plotted in µm as mean ± S.E. d As in A, wild type (WT) and Rgs2^−/− (KO) mice were exposed to aerosolized LPS for 3 and 24 h prior to fixing, sectioning and H&E staining. Representative images are shown. e Scoring of H&E staining images was performed as in A. Data (N = 7) are plotted as mean ± SE. f ASM thickness was measured and data (N = 11–14) are plotted as mean ± SE. In e and f, significance was tested between WT and KO using Mann–Whitney U test. No significant differences were found