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Lung Cytokines and ARDS*: Roger S. Mitchell Lecture

Thomas R. Martin, MD, FCCP
Author and Funding Information

*From the Medical Research Service, Seattle VA Medical Center, and the Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Washington School of Medicine, Seattle, WA. Supported in part by grants HL30542, A129103, and GM37696 from the National Institutes of Health, and the Medical Research Service of the Department of Veterans Affairs.

Correspondence to: Thomas R. Martin, MD, FCCP, Pulmonary Research Labs, 151L, Seattle VA Medical Center, 1660 S Columbian Way, Seattle, WA 98108; e-mail: trmartin@u.washington.edu



Chest. 1999;116(suppl_1):2S-8S. doi:10.1378/chest.116.suppl_1.2S
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Extract

The cellular and molecular basis for ARDS remains uncertain > 30 years after the original description of the syndrome. With the explosion of information about the involvement of cells and cytokines in inflammation, there has been intense interest in understanding the involvement of cytokines in the pathogenesis of ARDS. Cytokines are low-molecular-weight soluble proteins (generally < 30 kda) that transmit signals between cells. It is now clear that cytokine production is not limited to lymphoid and myeloid cells, and that cytokines produced by epithelial and mesenchymal cells amplify inflammatory responses in the lungs and other organs. Cytokines are produced in “cascades” in which the initial cytokine signals are amplified many-fold by target cells, such as epithelial cells, fibroblasts, and endothelial cells. Cytokines function in “networks” in which feedback occurs at many points to coordinate and regulate cytokine and cellular responses.


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