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Adhesion Molecules and Cellular Biomechanical Changes in Acute Lung Injury*: Giles F. Filley Lecture

Claire M. Doerschuk, MD; Joseph P. Mizgerd, ScD; Hiroshi Kubo, MD, PhD; Lan Qin, MD, PhD; Toshio Kumasaka, MD, PhD
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*From the Physiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA.

Correspondence to: Claire M. Doerschuk, MD, Physiology Program, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115-6021; e-mail: cdoersch@hsph.harvard.edu



Chest. 1999;116(suppl_1):37S-43S. doi:10.1378/chest.116.suppl_1.37S-a
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Extract

Neutrophils are thought to play an important role in the pathogenesis of ARDS.14 These patients often have a variety of inflammatory stimuli present within their lungs and circulating in their blood. The process through which these inflammatory mediators activate neutrophils and initiate their response occurs through a series of steps. First, the activated neutrophils sequester within the pulmonary microvasculature. They then adhere to the endothelium, a process most likely involving neutrophil-endothelial cell adhesion molecules. Neutrophils then migrate out of the vasculature into the lung parenchyma and airspace, usually in the presence of a lung injury or a chemotactic/haptotaxic gradient. Neutrophil-mediated injury to endothelial cells can occur during adhesion or emigration, although both these processes can occur in the absence of any discernible endothelial cell injury.


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