Pulmonary manifestations of heart failure (HF) are well-established in the clinic. The cystic fibrosis transmembrane regulator (CFTR) that presents with acquired dysfunction in several chronic lung diseases, has been suggested to be involved in HF progression in mice and men. We show that HF-associated reduction of pulmonary CFTR extends to non-alveolar macrophages in murine HF, which coincides with apparent tissue inflammation. Clinically approved CFTR correctors that were initially developed for the treatment of cystic fibrosis can reduce pulmonary inflammation during HF. This opens the door for repurposing existing CF therapeutics with long-term safety profiles to manage pulmonary complications during HF.