Fig. 3

a Before human albumin infusion. In ARDS, glycocalyx content is reduced and its function may be impaired depending on the stage of disease. Due to increased levels of pro-inflammatory mediators in the alveolar compartment, neutrophils are chemoattracted to the alveolar space, trespassing and causing damage to both endothelial cell junctions (e.g., VE-cadherin) and epithelial cell junctions (e.g., E-cadherin). Therefore, alveolar-capillary membrane damage increases, thus contributing to interstitial and alveolar edema. Activation of neutrophils in the alveolar space may promote the release of elastase and the production of neutrophil extracellular traps (NETs). Clot formation is increased, leading to aggregation of platelets into fibrin nets, which impair ventilation-perfusion ratio and decrease oxygenation. b After human albumin infusion. Human albumin is able to reduce levels of pro-inflammatory mediators in the alveolar compartment. Theoretically, this would reduce neutrophil attraction to the alveoli, thus reducing endothelial and epithelial cell damage and leading to decreased alveolar-capillary membrane permeability and lung edema. Human albumin is also able to maintain the glycocalyx connected to the luminal surface of endothelial cells. Finally, due to its heparin-like molecular structure, human albumin is able to reduce clot formation, which might improve ventilation-perfusion ratio and oxygenation