Table 1. Features of COPD that can/cannot be modelled in cigarette smoke-exposed mice.

Can be modelled	Cannot be modelled
BALF/lung inflammation, including neutrophilia, accumulation of macrophages and T-cells, and lymphoid aggregates/follicles Increase in BALF/lung inflammatory mediators, including cytokines, chemokines and proteases	Chronic bronchitisSevere disabling disease observed in GOLD stage 3 to 4
Increased oxidative stress
Emphysema
Small airway and vascular remodelling
Pulmonary hypertension
Mucus hypersecretion
Impaired lung function
Systemic co-morbidities (e.g. cardiac dysfunction and peripheral skeletal muscle wasting)
Increased BALF/lung inflammation in response to respiratory pathogens associated with infectious exacerbations
Persistence of BALF/lung inflammation following smoking cessation