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Am J Physiol Lung Cell Mol Physiol (January 5, 2007). doi:10.1152/ajplung.00248.2006
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Submitted on June 28, 2006
Accepted on December 28, 2006

Inhibition of JNK activation prolongs survival after smoke inhalation from fires

Olga L Syrkina1*, Deborah A Quinn2, Walter Jung3, Bin Ouyang2, and Charles A. Hales4

1 Department of Medicine, Massachusetts General Hospital, Pulmonary Critical Care Unit, United States; Harvard Medical School, Boston, Massachusetts, United States; Shriners Burn Hospital, Boston, Massachusetts, United States
2 Department of Medicine, Massachusetts General Hospital, Pulmonary Critical Care Unit, Boston, Massachusetts, United States; Harvard Medical School, Boston, Massachusetts, United States
3 Shriners Burn Hospital, Boston, Massachusetts, United States
4 Department of Medicine, Massachusetts General Hospital, Pulmonary Critical Care Unit, Boston, Massachusetts, United States; Harvard Medical School, Boston, Massachusetts, United States; Shriners Burn Hospital, Boston, Massachusetts, United States

* To whom correspondence should be addressed. E-mail: osyrkina{at}partners.org.

Initial injury from smoke inhalation is mainly to the trachea and bronchi, and is characterized by mucosal hyperemia and increased microvascular permeability, exfoliation of epithelial lining, mucous secretion, mucous plugging, and an acute inflammatory cell influx. In this study we explore the role of the c-Jun N-terminal protein kinase (JNK) pathway in smoke inhalation lung injury using a rat model of exposure to smoke from burning cotton. Male Spraque-Dawley rats were exposed to smoke from burning cotton for 15 minutes and one hour after injury a JNK inhibitor (SP600125) or vehicle was injected. We measured neutrophil influx, cytokine release, percent of apoptotic cells, airway plugging and survival. Administration of a JNK inhibitor (SP600125) one hour after smoke inhalation decreased airway apoptosis, mucous plugging, influx of inflammatory cells, the release of cytokines, and significantly prolonged animal survival (p<0.05). These in vivo data show the JNK pathway plays a critical role in smoke induced lung injury and offer an attractive therapeutic approach for this injury.




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