0995. Aspirin reduces neutrophilic pulmonary inflammation in a human model of acute respiratory distress syndrome induced by inhaled lipopolysaccharide

Acute respiratory distress syndrome (ARDS) is characterized by damage to the alveolar epithelial-endothelial barrier resulting in neutrophil influx and pulmonary oedema. The activation of platelet and secondary capture of neutrophils may play an important role in propagation of inflammation in ARDS [1]. Various animal studies have shown that aspirin therapy reduces pulmonary oedema and development of lung injury [2]. In observational studies, patients on aspirin therapy prior to hospital admission had a reduced incidence of ARDS [3]. By acetylating cyclooxygenase, aspirin inhibits platelet aggregation and generates anti-inflammatory molecules which modulate neutrophilic inflammation [4].