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

Crit Care. 2011;15(6):235. doi: 10.1186/cc10437. Epub 2011 Nov 30.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Carrier Proteins / physiology
  • Heat-Shock Proteins / physiology
  • Humans
  • Hyaluronic Acid / physiology
  • Immunity, Innate / physiology
  • NLR Family, Pyrin Domain-Containing 3 Protein
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic / physiology
  • Signal Transduction / physiology
  • Toll-Like Receptors / physiology
  • Ventilator-Induced Lung Injury / etiology*
  • Ventilator-Induced Lung Injury / metabolism
  • Ventilator-Induced Lung Injury / physiopathology


  • Carrier Proteins
  • Heat-Shock Proteins
  • NLR Family, Pyrin Domain-Containing 3 Protein
  • NLRP3 protein, human
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic
  • Toll-Like Receptors
  • Hyaluronic Acid