This phenotype has been shown in various models of CF including in the CFTR−/- pig and in mice using myeloid-specific deletion of Cftr, whether through use of bone marrow chimeras or LysMCre conditional models, demonstrating a role for CFTR-deficient macrophages in the aggravation of airway inflammation and thwarting of effective resolution in such mice following inflammatory or infectious challenge [17], [18], [19]. Here, CFTR is linked to cystic fibrosis.