Alveolar air–liquid interface (ALI)

The alveolar air–liquid interface (ALI) is the physiological boundary within the pulmonary alveoli where the respiratory epithelium interacts with the atmospheric air, facilitated by a thin layer of pulmonary surfactant (PubMed: 28811294). This interface is essential for efficient gas exchange, allowing oxygen to enter the bloodstream and carbon dioxide to be expelled, while serving as a critical defense barrier against inhaled pathogens and pollutants (StatPearls: NBK541005). In drug development, the ALI is widely recognized as a specialized in vitro culture model used to evaluate the safety, transport, and efficacy of inhaled therapeutics (PubMed: 31200408). Pathological disruption of this interface, characterized by increased permeability and surfactant dysfunction, is a hallmark of conditions such as acute respiratory distress syndrome (ARDS) and severe pneumonia (NIH: NHLBI). While the interface itself is a complex multicellular environment rather than a single molecular target, it is the functional site for various therapeutic interventions, including exogenous surfactant replacement and inhaled corticosteroids (PubMed: 25249413). Monitoring the health of the ALI often involves measuring transepithelial electrical resistance (TEER) or the expression of tight junction proteins to ensure barrier integrity.

Other names

Air-liquid interfaceAlveolar-capillary barrierLung air-liquid interfaceAlveolar-air interface

Exogenous surfactants reduce surface tension at the air-liquid interface to prevent alveolar collapse; other drugs may target specific receptors within the interface to restore barrier function.