Given our observation that pIgR-deficient mice have increased bacterial invasion across the mucosal surface of the airways, changes in microbial composition and a heightened inflammatory response, we postulated that endogenous bacterial flora in pIgR−/− mice could be responsible for driving persistent inflammation and COPD-like remodelling in the lungs of these mice. The gene discussed is PIGR; the disease is chronic obstructive pulmonary disease.