The acute respiratory distress syndrome (ARDS) is a severe form of respiratory failure with a mortality rate of approximately 40%. Despite advances in its supportive treatment such as lung protective ventilation or restrictive fluid management, no effective pharmacotherapy exists to treat ARDS. Emerging preclinical data indicates that excessive activation of the inflammasome-Caspase 1 pathway plays a key role in the development of ARDS. Tetracycline has anti-inflammatory properties via inhibiting inflammasome-caspase-1 activation. Since not much is known about the activation of the inflammasome in clinical ARDS, the purpose of this study is i) to investigate the the inflammasome-caspase-1 activation in clinical ARDS and ii) inhibit the innate immune response of alveolar leucocytes obtained by tetracycline from patients with ARDS

Inclusion Criteria:

• Age > 18 years
• Informed consent of the patient
• Diagnosis of ARDS for < 48 h

Exclusion Criteria:

• Age < 18 years
• Missing informed consent
• Immune therapy
• Autoimmune disease

Participants admitted to the Intensive Care Unit of the University Hospital of Bonn with an initial diagnosis of ARDS