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The Darc Side of Glycobiology in Acute Lung InjuryDarc Side of in Glycobiology Acute Lung Injury

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

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

Correspondence to: Jason D. Christie, MD, FCCP, Division of Pulmonary, Allergy and Critical Care Medicine, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania Perelman School of Medicine, 423 Guardian Dr, 719 Blockley Hall, Philadelphia, PA 19104; e-mail: jchristi@mail.med.upenn.edu


Funding/Support: Dr Christie is funded by the National Institutes of Health [HL081619].

Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr Christie is a coinvestigator on an National Institutes of Health-funded MAPGen study focusing on the ABO glycobiome in acute lung injury (HL108636), for which he receives 0.6 calendar months of salary support annually. 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 (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2012 American College of Chest Physicians


Chest. 2012;141(5):1132-1134. doi:10.1378/chest.12-0179
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Despite being common and carrying an estimated mortality in excess of 30%,1 acute lung injury (ALI) remains poorly understood. Few recent developments have improved the clinical management of affected patients. Significant advances in understanding the epidemiology and pathogenesis of ALI have been increasingly reported over the past 20 years; however, there are currently no pharmacologic interventions for the syndrome. To date, lung protective mechanical ventilation stands as the sole intervention to improve outcomes.2 Only a fraction of patients exposed to predisposing environmental insults, such as sepsis or trauma, develop ALI, leading to the hypothesis that genetic variation is a significant contributor to ALI susceptibility and outcomes. Over the past decade, candidate gene approaches have suggested genetic associations related to immune system function and pulmonary permeability.3 This relatively new focus on genetic risk has the potential to elucidate novel pathways involved in the pathogenesis of ALI and contribute to personalized medicine by identifying subgroups of patients that could uniquely benefit from targeted therapy. This is particularly true as newer, larger-scale genetic approaches are applied to ALI.4,5 Despite these findings, the understanding of the genetics of ALI remains in its infancy relative to other diseases, even within pulmonary medicine. The nature of the syndrome as sporadic and requiring a significant environmental insult complicates family-linkage approaches, and its heterogeneity leads to challenges in targeting the correct population and replicating results.

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