Fig. 1

Human IL-32γ prevents fibrosis in chronic asthma and bleomycin-induced pulmonary fibrosis models. a Evaluation of collagen deposits in the lungs of bleomycin-induced mice using Masson’s trichrome stain (original magnification: 100×). The quantification graphs of histological analysis in bleomycin-induced fibrosis groups. b Immunofluorescence analysis of α-SMA (green) expression in the lungs of bleomycin-induced mice. DAPI staining is blue (original magnification: 100×). c Hydroxyproline quantification. In the group with bleomycin-induced fibrosis treated with rIL-32γ (N = 5, B ± rIL-32γ), hydroxyproline levels tended to decrease compared to in the non-rIL-32γ-treated bleomycin-induced fibrosis model (N = 6, B) (32.40 ± 3.885 vs. 26.70 ± 1.287, P = 0.166). d Evaluation of collagen deposition in the lungs of chronic asthmatic mice using Masson’s trichrome stain (original magnification: × 200). e Immunofluorescence analysis of α-SMA (red) expression in the lungs of mice with chronic asthma. DAPI staining is blue (original magnification: × 200). f Hydroxyproline quantification graph. Similar results were obtained in each independent experiment, each using five mice per group (32.35 ± 1.752 vs. 24.20 ± 1.344, P = 0.010). *P ≤ 0.05