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Am J Physiol Lung Cell Mol Physiol 292: L984-L991, 2007. First published January 5, 2007; doi:10.1152/ajplung.00248.2006
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Inhibition of JNK activation prolongs survival after smoke inhalation from fires

Olga L. Syrkina,1,2 Deborah A. Quinn,1 Walter Jung,2 Bin Ouyang,1 and Charles A. Hales1,2

1Pulmonary and Critical Care Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, and 2Shriners Burn Hospital, Boston, Massachusetts

Submitted 28 June 2006 ; accepted in final form 28 December 2006

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 Sprague-Dawley rats were exposed to smoke from burning cotton for 15 min, and 1 h after injury a JNK inhibitor (SP-600125) or vehicle was injected. We measured neutrophil influx, cytokine release, percent of apoptotic cells, airway plugging, and survival. Administration of a JNK inhibitor 1 h after smoke inhalation decreased airway apoptosis, mucous plugging, influx of inflammatory cells, and the release of cytokines and significantly prolonged animal survival (P < 0.05). These in vivo data show that the JNK pathway plays a critical role in smoke-induced lung injury and offer an attractive therapeutic approach for this injury.

fire victims; apoptosis; c-Jun NH2-terminal kinase inhibitor


Address for reprint requests and other correspondence: O. L. Syrkina, Pulmonary and Critical Care Unit, Massachusetts General Hospital, 55 Fruit St., Bulfinch 148, Boston, MA 02114 (e-mail: osyrkina{at}partners.org)




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