RhCC16 limited the progression of emphysema, small airway fibrosis, and chronic bronchitis-like disease in WT and Cc16–/– mice partly by reducing pulmonary inflammation (reducing myeloid leukocytes and/or increasing regulatory T and/or B cells) and alveolar septal cell apoptosis, reducing NF-κB activation in CS-exposed Cc16–/– lungs, and rescuing the reduced Foxj1 expression in CS-exposed Cc16–/– lungs. Here, FOXJ1 is linked to pulmonary emphysema.