Acute Respiratory Distress Syndrome: Role of Oleic Acid-Triggered Lung Injury and Inflammation

Figure 1

Effects of oleic acid in acute respiratory distress syndrome. Oleic acid induces damage in epithelial and endothelial cells, with increased permeability and protein-rich edema, with denuded areas in alveoli forming a hyaline membrane. Oleic acid induces apoptosis or necrosis in alveolar type I or type II cells (d), depending on the insult origin. Alveolar macrophages (b) act as sentinels triggering the immune response and produce chemotactic and inflammatory mediators. Chemoattractant mediators produced by alveolar macrophages and epithelial and endothelial cells induce increased adhesion molecules such as VCAM-1, selectins, and integrins, favoring the inflammatory cell infiltration. Neutrophils (a) are first cells migrating to lung and their excessive recruitment contributes to the lung pathology and they produce and release other inflammatory mediators and other molecules such as proteases and elastase. Aquaporin 5 is (c) a water channel responsible for moving water from the alveoli to the lung interstitium, AO-induced lung injury could advent via intrapulmonary or extrapulmonary. In case of extrapulmonary ARDS the main target will be endothelial cells and leukocytes inducing endothelial cell death (e). Similar to humans, OA induces lung hemorrhage. OA inhibits ENaC and NKA inducing and/or avoiding edema fluid clearance. ENaC: epithelial sodium channel; CFTR: cystic fibrosis transmembrane conductance regulator; NKA: Na/K-ATPase; VCAM-1: vascular cell adhesion molecule 1.