Increased susceptibility to airway bacteria caused by an immune system defect may explain why patients with COPD experience persistent lung inflammation and disease progression even after they stop smoking, researchers reported.

In a mouse model, the researchers showed that lacking the key mucus secretion antibody known as secretory immunoglobulin A (IgA) increased susceptibility to bacterial infection, which mimicked the lung damage and persistent inflammation characteristic of COPD in the aging mice. Treatment of the IgG-deficient mice with the anti-inflammatory COPD drug roflumilast halted the lung damage.