COPD describes a group of conditions that are characterized by loss of the functional capacity of the lungs, which is due to reduced and obstructed airflow.1 This disease exerts a large and increasing health burden worldwide and is often caused by exposure to tobacco smoking. Although primarily considered a respiratory disease, there is growing clinical interest in secondary organ manifestations of COPD, particularly in the GI tract. Indeed, GI disease is more prevalent in patients with COPD than in healthy populations.2 A population-based cohort study performed by Ekbom et al,3 showed a 2.72 times higher risk of Crohn’s disease (an inflammatory bowel disease) in COPD sufferers than that in healthy control subjects, greater than the risk reported for smoking alone. Specific intestinal complications include atrophic gastritis and nutritional absorption deficiency in the small intestine.4,5 Thus, there is a clear link between inflammatory diseases in the respiratory and intestinal systems. However, there have been surprisingly few research studies that have investigated the nature of the cross talk involved, and while several mechanisms have been proposed,6 to date there have been few studies that have aimed to elucidate these connections.