Gastroesophageal reflux (GER) is a potential trigger of asthma. The esophagus and lung interact through a variety of mechanisms. Esophageal acid-induced bronchoconstriction can be provoked by a vagally mediated reflex, whereby acid in the distal esophagus produces airway responses; by neural enhancement of bronchial reactivity, whereby esophageal acid augments airway hyperresponsiveness; or by microaspiration, in which small amounts of esophageal acid in the upper airway cause significant airway responses. Interestingly, even in the microaspiration model, the vagus nerve plays a significant role. Neurogenic inflammation in the lung may occur with either vagally mediated mechanisms or with microaspiration. The prevalence of reflux symptoms, esophagitis, and abnormal esophageal acid contact time is higher in patients with asthma than in control populations. Potential mechanisms, whereby asthma may predispose to the development of GER, include autonomic dysregulation, an increased pressure gradient differential between the thorax and the abdomen, a high prevalence of hiatal hernia, alterations in crural diaphragm function, and bronchodilator medication use. Further research will help define how the esophagus and lung interact.