Fig. 9: Effects of tobacco smoke exposure in WT and Trpml3^−/− mice (Mcoln3^tm1.1Jga).

a Lung function measurements were performed using the SCIREQs FlexiVent System in analogy to experiments shown in Fig. 2. Elastance and Compliance in Trpml3^−/− mice are changed in the direction of an emphysematous lung, both under filtered air (FA) and under cigarette smoke (CS). b Quantification of airspace enlargement as mean linear chord length. Lung tissue sections from 6–8 mice per group were analysed. Each dot corresponds to one biologically independent lung tissue sample. Average values are mean values ± SEM, each. *p < 0.05, **p < 0.01, ***p < 0.001; One-way ANOVA followed by Tukey’s post hoc test. c Representative images of H&E-stained lung tissue sections (as quantified in b) from mouse lungs (BL6 WT and Trpml3^−/−) exposed to CS or FA showing the respective extent of airspace enlargements. Scale bar 100 µm. d Transcriptomics data of single-cell suspensions from female and WT whole mouse lungs that were exposed to FA or CS for 2 or 6 months. Dot plot shows the percentage of cells expressing Mcoln3 using dot size and the average expression level of Mcoln3 coded by color grading. e mRNA expression level of MCOLN3 in publicly available transcriptomics datasets obtained from the lungs of COPD patients with smoking history compared to healthy smokers (GSE27597), and in macrophages (MΦ) isolated from the bronchoalveolar lavage (BAL) of smokers compared to nonsmokers (GSE8823 and GSE2125), one single dot per person. Expression levels were normalized to the representative control groups. FC fold change. **p < 0.01, ***p < 0.001, ****p < 0.0001; two-tailed Mann-Whitney test. Source data are provided as a Source Data file.