Acute respiratory distress syndrome (ARDS) is a life-threatening form of respiratory failure characterised by widespread inflammatory lung injury. Damage to the delicate alveoli and microvasculature leads to significant alveolar oedema, impaired gas exchange and, ultimately, hypoxaemia [1]. ARDS can be triggered by a variety of different insults, which can be either infectious or non-infectious in nature, and common causes include pneumonia, sepsis, aspiration, noncardiogenic shock, trauma, blood transfusion and inhalation injury [1]. The initial insult leading to ARDS may directly or indirectly involve the lung (e.g. trauma to the lung versus extremities), yet a robust immune response is observed in the lung in both cases. ARDS affects ∼10% of patients admitted to the intensive care unit and 23% of those requiring mechanical ventilation, and has a mortality rate of 35–46% [2]. There are no therapies available for these patients and, as such, understanding the underlying mechanisms of ARDS is key to future interventional therapy.