Fig. 4

Intraperitoneal administration of LGp40 inhibited M2 macrophage accumulation and promoted accumulation of M1 macrophages in the lung of mice with HDM-induced asthma. Lung sections were immunostained with a iNOS and b arginase-1 antibodies and then reacted with diaminobenzidine (scale bars = 200 and 100 μm). The iNOS-positive cells (blue arrows) were counted in every lobe per group, and the average numbers were calculated. The arginase-1-positive cells (red arrows) were counted in ×200 microscopic fields per group, and the average numbers were calculated (n = 6 mice, **p < 0.01, one-way ANOVA with Bonferroni multiple comparison test). M1 and M2 cell percentages c in single lung suspensions and d in peritoneal cavity were determined using flow cytometry analysis (n = 15 mice, *p < 0.05 and **p < 0.01, two-way ANOVA with Bonferroni multiple comparison test). e IL-4- and IL-13-stimulated BMDM were incubated with naïve Th cells in the presence of LGp40 and CDp40. IL-4⁺ Th2 cell populations were determined using flow cytometry analysis (n = 6 mice, *p < 0.05 and **p < 0.01, one-way ANOVA with Bonferroni multiple comparison test). Results comprise pooled data from three independent experiments