Platelets in the pathogenesis of acute respiratory distress syndrome

Abstract

Platelets have an emerging and incompletely understood role in a myriad of host immune responses, extending their role well beyond regulating thrombosis. Acute respiratory distress syndrome is a complex disease process characterized by a range of pathophysiologic processes including oxidative stress, lung deformation, inflammation, and intravascular coagulation. The objective of this review is to summarize existing knowledge on platelets and their putative role in the development and resolution of lung injury.

Keywords: ALI; ARDS; aspirin; lung injury; platelet.

Fig. 1.

Mechanisms by which platelets may contribute to the development and resolution of acute respiratory distress syndrome (ARDS). IL-6, interleukin-6; TNF, tumor necrosis factor; NF-кB, nuclear factor-к-light-chain-enhancer of activated B cells; ASA, aspirin; LXs, lipoxins; ATLs, aspirin-triggered lipoxins; HO-1, heme oxygenase-1; ICAM-1, intercellular adhesion molecule; CCL-5, chemokine (C-C motif) ligand-5; CXCL4, chemokine (C-X-C motif) ligand-4; vWF, von-Willebrand factor; NETs, neutrophil extracellular traps.