The activity of CFTR was regulated by the intracellular cAMP concentration.24 We have previously demonstrated that PDE4 (which degraded intracellular cAMP) could modulate [Cl−]i and promote the ongoing epithelial inflammation during bacterial infections.23 Here, we have further shown that the mRNA expression levels of PDE4C and PDE4D were upregulated at 12 h and thereafter following N protein stimulation in BEAS-2B cells (Fig. 5a and Supplementary Fig. S6). Here, PDE4D is linked to bacterial infectious disease.