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ALI and its exacerbated form, acute respiratory distress syndrome (ARDS), are categorized by their symptoms and severity according to the Berlin Definition.[1] ALI is characterized by increased permeability of the alveolar-capillary barrier, which consequently leads to lung edema with pulmonary infiltrates and hypoxemia.[2],[3] ALI patients manifest significant pulmonary inflammation that causes flooding of the pulmonary alveoli, resulting in obstructed gas exchange and consequent hypoxemia.
Studies had proved that TNF-a derived TIP peptide inhalation could reduce the extravascular lung water index as well as increase the PaO(2)/FiO(2) ratio.[21],[22] The protective role of TNF-derived TIP peptide lies in that through binding to epithelial sodium channel-a, it is able to strengthen the barrier function and maintain permeability of the alveolar-capillary barrier.[23]
Moreover, the alveolar epithelium damage will lead to an increase in the permeability of the alveolar-capillary barrier, which in combination with changes in hydrostatic and oncotic pressures, might lead to the formation of pulmonary edema.[44],[45]