Fig. 3

Blockade of NLRP3 inflammasome or IL-1β abrogates airway inflammation in miR-223^−/− mice. OVA/CFA was administrated to WT mice and miR-223^−/− mice on day 0. miR-223^−/− mice received the inhibitor of NLRP3, MCC950 (200 mg/kg, i.p.) and IL-1β receptor antagonist, anakinra (50 mg/kg, i.p.) or PBS after each challenge, respectively. Mice were euthanized 24 h after the final treatment. a Representative micrographs of lung H&E staining a-d and PAS staining e-h from different groups after treatment (200× magnification). b-c Semi-quantification of lung inflammatory score and Apas⁺/Pbm was performed. n = 6–8 mice/group; statistical significance was determined by ANOVA. d Number of total inflammatory cells, neutrophils, eosinophils, and lymphocytes was calculated in BALF after treatment. n = 6–8 mice/group; statistical significance was determined by ANOVA. e AHR was determined by lung resistance after treatment. n = 6–8 mice/group. Statistical significance was determined by ANOVA. f-n The levels of Th2-associated cytokines (IL-4, IL-5, IL-13), Th17-associated cytokines (IL-17A, IL-22, IL-23), Th1-associated cytokine (IFN-γ), IL-1β, and IL-18 in BALF were measured by ELISA after treatment. n = 6–8 mice/group; statistical significance was determined by ANOVA. All data were expressed as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001