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Interactions between Mechanical and Biological Processes in Acute Lung Injury

¹ Medical Research Service of the VA Puget Sound Medical Center, and the Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Washington, Seattle, Washington

Correspondence and requests for reprints should be addressed to Thomas R. Martin, M.D., Pulmonary Research Laboratory, 151L, VA Puget Sound Medical Center, 1660 S. Colombian Way, Seattle, WA 98108. E-mail: trmartin{at}u.washington.edu

ABSTRACT

Human studies and animal models suggest that mechanical as well as biological processes contribute to acute lung injury. While mechanical stresses and bacterial products can directly alter the endothelial and epithelial barriers in the lungs, a growing body of evidence suggests that synergistic interactions between low levels of mechanical stress and bacterial products in the lungs can cause or exacerbate acute lung injury. New approaches to disrupting these synergistic interactions between mechanical stress and innate immunity have the potential to reduce the incidence or improve the outcome of acute lung injury in humans.

Key Words: lung injury • epithelium • VILI • apoptosis