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Published ahead of print on May 13, 2004, doi:10.1164/rccm.200401-023OC

Am. J. Respir. Crit. Care Med., Volume 170, Number 6, September 2004, 613-620

A more recent version of this article appeared on September 15, 2004
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Submitted on January 12, 2004
Accepted on May 7, 2004

Inhaled Carbon Monoxide Confers Anti-inflammatory Effects Against Ventilator-induced Lung Injury

Tamas Dolinay1, Maria Szilasi2, Mingyao Liu3, and Augustine M.K. Choi4*

1 Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA, United States; Department of Pulmonary Medicine, University of Debrecen, Debrecen, Hungary, 2 Department of Pulmonary Medicine, University of Debrecen, Debrecen, Hungary, 3 Thoracic Surgery Resarch Laboratory, University of Toronto, Toronto General Hospital, Toronto, ON, Canada, 4 Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA, United States

* To whom correspondence should be addressed. E-mail: choiam{at}.upmc.edu.

Ventilator-induced lung injury is a major cause of morbidity and mortality in intensive care units. The stress inducible gene product, heme oxygenase-1 and carbon monoxide (CO), a major by-product of heme oxygenase catalysis of heme, have been shown to confer potent anti-inflammatory effects in models of tissue and cellular injury. In this study, we observed increased expression of heme oxygenase-1 mRNA and protein in a rat model of ventilator-induced lung injury. To assess the physiological function of heme oxygenase-1 induction in ventilator-induced lung injury, we determined whether low concentration of inhaled CO could serve to protect the lung against ventilator-induced lung injury. Low concentration of inhaled CO significantly reduced tumor necrosis factor-{alpha} levels and total cell count in lavage fluid, while simultaneously elevating levels of anti-inflammatory interleukin-10 levels. To better characterize the mechanism of CO-mediated anti-inflammatory effects, we examined key signaling pathways, which may mediate CO-induced anti-inflammatory effects. We demonstrate that inhaled CO exerts anti-inflammatory effects in ventilator-induced lung injury via the p38 mitogen-activated protein kinase pathway but independent of AP-1 and NF-{kappa}B pathways. Our data lead to a tempting speculation that inhaled CO might be useful in minimizing ventilator-induced lung injury.
Key words: p38 MAPK, cytokines, heme oxygenase-1




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