Fig. 6

HDM makes the lung TME conducive to tumor growth and IL-1β neutralization abrogates this effect. A Representative pictures of H&E-stained lung sections from Kras^G12D mice (n = 3 mice/group) treated i.n with VEH or HDM as shown in Fig. 2A, or i.n with HDM and i.p with a neutralizing anti-IL-1β Ab as shown in Supplemental Fig. 6A. The whole lung of one representative mouse from each experimental group is shown. B mIF staining of lung sections of the mice shown in A. Overlay (top) and single colors (bottom). DAPI nuclear staining (blue), F4/80 (magenta), Ki-67 (cyan) and PanCK (yellow). C Selected ROI#1 (left) and ROI#2 (right) from the H&E-stained lung section of the HDM-treated mouse in A showing inflammatory cell infiltrates and a representative grade 3 lesion, respectively. D IHC staining for TTF-1 of the same ROI#1 and ROI#2 as in C. E Corresponding mIF images showing high F4/80 immunoreactivity in parenchymal lung tissue (left, ROI#1), and high Ki-67 immunoreactivity in tumor cells as well as peritumoral F4/80⁺ cell infiltration (right, ROI#2). Overlay (top) and single colors (bottom). F Quantification of F4/80⁺ cells in whole lungs. G Quantification of Ki-67.⁺ cells in tumor areas. Scale bars, 2 mm (whole lungs), 0.4 mm (ROI#1), and 0.8 mm (ROI#2). Data are representative of one (A, C, and D) or two (B, E–G) independent experiments and are presented as mean ± SEM. Statistical significance was assessed by one-way ANOVA with post hoc Bonferroni’s test. n.s: non-significant, * P < 0.05, ** P < 0.01