Moreover, in an LPS-induced ALI/ARDS model, LPS stimulates immune cells (e.g., macrophages and neutrophils) to produce different mediators, including cytokines, such as TNF-α and IL-1β, which downregulate ENaC-α expression and/or activity in alveolar epithelial cells and impair AFC capacity [77, 78]. This evidence concerns the gene IL1B and acute respiratory distress syndrome.