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Review

Bench-to-bedside review: Damage-associated molecular patterns in the onset of ventilator-induced lung injury

Maria T Kuipers1234*, Tom van der Poll34, Marcus J Schultz12 and Catharina W Wieland12

Author Affiliations

1 Laboratory of Experimental Intensive Care and Anesthesiology, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands

2 Department of Intensive Care, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands

3 Center of Experimental and Molecular Medicine, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands

4 Center of Infection and Immunity, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands

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Critical Care 2011, 15:235  doi:10.1186/cc10437

Published: 30 November 2011

Abstract

Mechanical ventilation (MV) has the potential to worsen pre-existing lung injury or even to initiate lung injury. Moreover, it is thought that injurious MV contributes to the overwhelming inflammatory response seen in patients with acute lung injury or acute respiratory distress syndrome. Ventilator-induced lung injury (VILI) is characterized by increased endothelial and epithelial permeability and pulmonary inflammation, in which the innate immune system plays a key role. A growing body of evidence indicates that endogenous danger molecules, also termed damage-associated molecular patterns (DAMPs), are released upon tissue injury and modulate the inflammatory response. DAMPs activate pattern recognition receptors, may induce the release of proinflammatory cytokines and chemokines, and have been shown to initiate or propagate inflammation in non-infectious conditions. Experimental and clinical studies demonstrate the presence of DAMPs in bronchoalveolar lavage fluid in patients with VILI and the upregulation of pattern recognition receptors in lung tissue by MV. The objective of the present article is to review research in the area of DAMPs, their recognition by the innate immune system, their role in VILI, and the potential utility of blocking DAMP signaling pathways to reduce VILI in the critically ill.