Fig 1: FGF10 inhibits MLE12 pyroptosis induced by LPS‐primed iBMDMs. (A) Flow cytometry quantification of FGFR2b⁺ cells in alveolar epithelial cells (EPCAM⁺), macrophages (CD11b⁺F4/80⁺) and neutrophils (CD11b⁺Ly6G⁺). (B) Schematic representation of MLE12 and iBMDMs co‐culture system. Cells were pre‐treated with PBS/FGF10 (100 ng/mL) for 6 h and then interfered with LPS (1 µg/mL) for 6 h. (C) Cell viability assessed by CCK‐8 assay (left) and PI⁺ dead cell proportion (right). (D) Representative PI staining images (red: dead cells, scale bar: 100 µm). (E) Quantification of PI⁺ MLE12 cells. (F) Detection of LDH level in MLE12 cells. (G) Western blot analysis of RIPK1, caspase‐8, caspase‐3 and GSDME in co‐cultured MLE12 cells. Statistical analysis of protein activation of RIPK1, caspase‐8, caspase‐3 and GSDME (normalised to tubulin). (H) qRT‐PCR analysis of Ripk1, Casp8, Casp3, Gsdme and pro‐inflammatory cytokines (Tnfa, Il6, Il1b, Il18) in MLE12 cells. Statistical significance was determined by one‐way ANOVA with Tukey's post hoc test. Four independent experiments are carried out. Data are shown as mean ± SD (n = 4, *p < .05, **p < .01, ***p < .001).