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New mouse models have enabled studies of the pathogenesis of infectious exacerbations of airway inflammation.Early life infections alter immunity and lung structure to increase AAD severity.Later life infections alter immune phenotype and induce severe steroid-resistant AAD.Infection in experimental COPD increases inflammation and remodeling and alters infection clearance.Understanding disease pathogenesis enables the ID and testing of new therapeutics.Airway inflammation underpins the pathogenesis of the major human chronic respiratory diseases. It is now well recognized that respiratory infections with bacteria and viruses are important in the induction, progression and exacerbation of these diseases. There are no effective therapies that prevent or reverse these events. The development and use of mouse models are proving valuable in understanding the role of infection in disease pathogenesis. They have recently been used to show that infections in early life alter immune responses and lung structure to increase asthma severity, and alter immune responses in later life to induce steroid resistance. Infection following smoke exposure or in experimental chronic obstructive pulmonary disease exacerbates inflammation and remodeling, and worsens cystic fibrosis. Further exploration of these models will facilitate the identification of new therapeutic approaches and the testing of new preventions and treatments.