Fig. 9
Neutrophil-derived Il1r2 promotes M2 polarization in ALI. (A) Representative immunohistological staining images demonstrating Il1r2 expression in the lungs of mice. Scale bar, 100 μm. (B) Quantification of Il1r2 expression levels based on immunohistochemistry (n = 3 mice per group) (C) Immunofluorescence staining was used to verify Il1r2 secretion by neutrophils in ALI samples. Scale bars: 100 μm and 20 μm. (D) Quantification of Il1r2 expression based on immunofluorescence (n = 3 mice per group). (E) Violin plot showing the expression levels of Cd86 and Cd163 in ALI and control samples. (F) Immunoblotting analysis of Il1r2 expression in lung tissues from Con, Con + Il1r2-OE, ALI, and ALI + Il1r2-OE mice (n = 3 mice per group). (G) Densitometric quantification of Il1r2 protein levels in (F). (H) RT-qPCR analysis of Il1r2 mRNA expression in lung tissues from Con + AAV9-GFP, Con + AAV9-Il1r2, ALI + AAV9-GFP, and ALI + AAV9-Il1r2 mice (n = 3 mice per group). (I–K) Immunoblotting and quantification of iNOS and CD68 protein levels in lung tissues from Con + AAV9-GFP, Con + AAV9-Il1r2, ALI + AAV9-GFP, and ALI + AAV9-Il1r2 mice (n = 3 mice per group). (L–N) Immunoblotting and quantification of CD206 and Arg-1 expression in lung tissues from Con + AAV9-GFP, Con + AAV9-Il1r2, ALI + AAV9-GFP, and ALI + AAV9-Il1r2 mice (n = 3 mice per group). (O–Q) Immunoblotting and quantification of TNF-α and IL-1β expression in lung tissues from Con + AAV9-GFP, Con + AAV9-Il1r2, ALI + AAV9-GFP, and ALI + AAV9-Il1r2 mice (n = 3 mice per group). All data are expressed as mean ± SD, P < 0.05 were considered statistically significant differences. *P < 0.05; **P < 0.01; ***P < 0.005. Two-tailed unpaired Student’s t-test for two groups or one-way ANOVA for three groups or more. Con, Control; ALI, Acute Lung Injury.
