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Linking Genetics to ARDS PathogenesisPlatelets, Genetics, and ARDS: The Role of the Platelet

John P. Reilly, MD, MSCE; Jason D. Christie, MD, MSCE
Author and Funding Information

From the Division of Pulmonary, Allergy and Critical Care Medicine, Center for Clinical Epidemiology and Biostatistics, Perelman School of Medicine at the University of Pennsylvania.

CORRESPONDENCE TO: Jason D. Christie, MD, MSCE, Division of Pulmonary, Allergy and Critical Care Medicine, Center for Clinical Epidemiology and Biostatistics, Perelman School of Medicine at the University of Pennsylvania, 717 Blockley Hall, 423 Guardian Dr, Philadelphia, PA 19104; e-mail: jchristi@upenn.edu


FINANCIAL/NONFINANCIAL DISCLOSURES: The authors have reported to CHEST the following conflicts: Dr Christie has received funding from the National Institutes of Health to study glycobiology and ARDS. Dr Reilly has reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;147(3):585-586. doi:10.1378/chest.14-2701
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ARDS is a complex syndrome, characterized by damage to the alveolar-capillary barrier resulting in increased permeability in the setting of an amplified inflammatory response. The role of the activation of clotting pathways in this process has been increasingly recognized, including the significant impact of platelets on ARDS pathogenesis.1-3 In a steady state, inactive platelets circulate in blood and promote endothelial barrier integrity.4 However, in the setting of critical illnesses (eg, sepsis), several overlapping mechanisms activate platelets, resulting in platelet aggregation, platelet-leukocyte complex formation, and release of the granule contents of the platelet cell, including molecules that enhance inflammation and cell adhesion. While platelet-mediated thrombosis in the lungs has been implicated in ARDS pathogenesis, the activation of circulating platelets results in a host of other inflammatory effects contributing to ARDS development, including augmented neutrophil migration and increased endothelial barrier permeability.3

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