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Acute respiratory distress syndrome (ARDS), the most severe form of acute lung injury, is a devastating clinical syndrome with a high mortality rate (30–60%) (refs ). Predisposing factors for ARDS are diverse^, and include sepsis, aspiration, pneumonias and infections with the severe acute respiratory syndrome (SARS) coronavirus^,. At present, there are no effective drugs for improving the clinical outcome of ARDS^,,. Angiotensin-converting enzyme (ACE) and ACE2 are homologues with different key functions in the renin–angiotensin system^,,. ACE cleaves angiotensin I to generate angiotensin II, whereas ACE2 inactivates angiotensin II and is a negative regulator of the system. ACE2 has also recently been identified as a potential SARS virus receptor and is expressed in lungs^,. Here we report that ACE2 and the angiotensin II type 2 receptor (AT₂) protect mice from severe acute lung injury induced by acid aspiration …