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Initiation and Tolerance to Acute Lung Injury*: Yin-Yang Mechanisms Involving Interleukin-1

Rosa Faust-Chan; Brooks Hybertson, PhD; Sonia C. Flores, PhD; Richard M. Wright, PhD; John E. Repine, MD
Author and Funding Information

*From the Webb-Waring Institute for Cancer, Aging, and Antioxidant Research at the University of Colorado Health Sciences Center, Denver, CO.

Correspondence to: John E. Repine, MD, 4200 E Ninth Ave, Box C322, Denver, CO



Chest. 1999;116(suppl_1):102S-103S. doi:10.1378/chest.116.suppl_1.102S
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Extract

ARDS remains a medical problem of considerable importance. Recent clinical trials, unfortunately, have failed to identify any therapeutic agent that has the potential of reducing the consequences of this devastating condition.

A persistent concept in the sought-after understanding of the pathogenesis of ARDS has been that an exaggerated systemic inflammatory process contributes to the pulmonary dysfunction and the multiorgan failure that subsequently characterize the syndrome. This inflammatory process is in part reflected by the increased numbers of neutrophils and increased levels of cytokines in the lung lavages of affected ARDS patients compared with control subjects. Moreover, numerous in vitro and animal studies have provided extensive evidence that suggests that neutrophils and cytokines can cause endothelial cell damage and produce lung leak abnormalities that are consistent with the lung abnormalities that occur in ARDS patients.


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