Fig. 1: ACE2 expression is reduced in CF airway epithelia.

a, b Quantification of ACE2 mRNA expression by qPCR in lysates collected from well-differentiated hNECs and hBECs, grown at the air-liquid interface. Epithelia were derived from a pool of fourteen healthy donors (hNEC) and two CF patients (CF-hNEC) (a), or from six healthy donors (hBEC) and six CF patients (CF-hBEC) (b). The genotypes of the patients enrolled in this study are reported in Supplementary Table 1. Data are shown as the mean ± SEM of independent experiments (n = 4 and n = 6 for hNEC and hBEC, respectively). c Representative western blot analysis of protein extracts from differentiated hNECs grown at the air–liquid interface obtained from a pool of fourteen healthy control subjects versus CF-hNECs obtained from two F508del-CFTR homozygous CF patients. d Western blot analysis of ACE2 in differentiated hBEC grown at the air–liquid interface obtained from four CF patients compared with four healthy donors. Normal hBEC were additionally incubated in the presence (+) or absence (−) of 5 μM CFTR inhibitor CFTR(inh)-172 for 24 h. e Densitometry analysis (% of β-actin expression) of two independent experiments (n = 2), conducted as reported in (c). f Densitometry analysis (% of β-actin expression) of four independent experiments (n = 4) performed in protein extracts from hBEC, as reported in panel (d). Data represented in panels e, f are shown as the mean ± SEM. Normal distribution was confirmed using the Shapiro–Wilk test before running two-tailed Student’s t-test (a, b, f), which has been reported in the scatter plot with bars (*p < 0.05). Source data are provided as a Source Data File.