Fig. 2

ACE2 gene expression associations in SPIROMICS. a–d Box plots showing that ACE2 log₂ gene expression (x-axis) was increased in association with current but not former smoking as compared to never smokers (a), obesity (b, validated in the MAST and SARP cohorts, Additional file 3: Figure S2a-b), hypertension (c, adjustments include anti-hypertensive treatment, validated in SARP, Additional file 3: Figure S3a, data not collected in MAST), and female sex (d, not replicated in either MAST or SARP, Additional file 2: Table S1A). e Scatterplots showing that ACE2 gene expression was increased in association with higher levels of our previously validated gene signatures of the airway epithelial response to interferon (left panel, replicated in SARP) and to IL-17 inflammation (right panel, replicated in MAST and SARP) after adjusting for smoking status (Additional file 2: Table S1B). f Box plots showing that ACE2 Exon 1c, which contributes to the truncated ACE2 transcript was differentially increased in association with our interferon signature while Exons 1a and 1b that contribute to the full length ACE2 transcript were not. P values indicated by: **** < 0.0001, *** < 0.001, ** < 0.01, * < 0.05, ns = not significant in linear models adjusted for covariates. In a–d and f, the boxes denote the interquartile range, the center line denotes the median, and whiskers denote the interquartile range × 1.5