Inhibition of receptor for advanced glycation end-products (RAGE) improves alveolar fluid clearance and lung injury in a mouse model of acute respiratory distress syndrome (ARDS)

Rationale The receptor for advanced glycation end-products (RAGE) is a transmembrane multipattern receptor abundantly expressed on the basal surface of alveolar type (AT) I cells. RAGE is implicated in ARDS-associated alveolar inflammation [1,2], but its precise roles in lung injury remain unknown. It has been shown recently that RAGE axis could impact alveolar fluid clearance (AFC) through the modulation of epithelial sodium channels [3]. In mouse models of sepsis and of ARDS, treatment with anti-RAGE monoclonal antibody decreased mortality, and treatment with recombinant soluble RAGE (sRAGE, acting as a decoy receptor) was associated with improved lung injury.