Acute respiratory distress syndrome: new pathophysiological insights

Acute respiratory distress syndrome (ARDS) remains a major cause of critical illness with high morbidity and mortality. Despite advances in supportive care, targeted therapies have failed, in part due to an incomplete understanding of alveolar immune dysregulation. This review provides a timely synthesis of emerging mechanisms in alveolar immune dysregulation that underlie the development and persistence of ARDS.

Recent studies highlight the role of neutrophil heterogeneity, alveolar macrophage-derived extracellular vesicle signaling, and epithelial barrier dysfunction in driving hyperinflammation and susceptibility to secondary infections. Mechanical ventilation strategies, particularly those influencing driving pressure, further shape the alveolar immune environment. Cross-talk between immune cells and mechanical forces appears central to the pathogenesis of sustained lung injury.

Understanding the dynamic interplay between alveolar immune responses and secondary insults is critical for the development of precision medicine approaches in ARDS. Future research should prioritize the identification of compartment-specific biomarkers and therapeutic targets aimed at restoring immune balance and preventing nonresolving lung injury.