Related Experiment Video
Updated: Nov 11, 2025
A Model of Self-limited Acute Lung Injury by Unilateral Intra-bronchial Acid Instillation
Published on: August 30, 2019
A role for bronchial epithelial autotaxin in ventilator-induced lung injury
Ioanna Nikitopoulou1, Ioanna Ninou2, Nikolaos Manitsopoulos1
11st Department of Critical Care Medicine & Pulmonary Services, GP Livanos and M Simou Laboratories, National and Kapodistrian University of Athens Medical School, Evangelismos Hospital, 45, Ipsilantou Street, Athens, Greece.
Background:
The pathophysiology of acute respiratory distress syndrome (ARDS) may eventually result in heterogeneous lung collapse and edema-flooded airways, predisposing the lung to progressive tissue damage known as ventilator-induced lung injury (VILI). Autotaxin (ATX; ENPP2), the enzyme largely responsible for extracellular lysophosphatidic acid (LPA) production, has been suggested to play a pathogenic role in, among others, pulmonary inflammation and fibrosis.
Methods:
C57BL/6 mice were subjected to low and high tidal volume mechanical ventilation using a small animal ventilator: respiratory mechanics were evaluated, and plasma and bronchoalveolar lavage fluid (BALF) samples were obtained. Total protein concentration was determined, and lung histopathology was further performed RESULTS: Injurious ventilation resulted in increased BALF levels of ATX. Genetic deletion of ATX from bronchial epithelial cells attenuated VILI-induced pulmonary edema.
Conclusion:
ATX participates in VILI pathogenesis.
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