Since pulmonary exacerbations are commonly triggered by infections, the autophagy dysfunction seen in these chronic conditions plays a role in the pathogenesis of this state via the mechanisms discussed above. A common pathogen that colonizes the lungs of individuals with chronic respiratory diseases and can lead to exacerbations is P. aeruginosa [4,31,44,58,173,178]. Studies have demonstrated that defects in CFTR impair the ability of cells to clear P. aeruginosa infections via autophagy, especially in patients with CF [22,40,53]. Furthermore, it has been shown that the induction of autophagy is able to ameliorate autophagy dysfunction and promote the clearance of P. aeruginosa infections [35,45,58]. As previously mentioned, CS exposure can also cause CFTR dysfunction, where a recent investigation demonstrated that CS exposure decreased CFTR expression while a treatment of CS-exposed macrophages with the autophagy inducer fisetin, which works by modulating autophagosome degradation, significantly recovered CFTR expression [35]. This same investigation showed that the CS-induced inhibition of CFTR decreased the clearance of P. aeruginosa [35]. This impaired clearance was then alleviated by autophagy induction with fisetin, supporting the findings of other previously mentioned studies [35]. Hence, CFTR-autophagy dysfunction in chronic lung diseases such as CF and COPD leads to P. aeruginosa exacerbations.