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Published ahead of print on November 25, 2003, doi:10.1164/rccm.200305-660OC

Am. J. Respir. Crit. Care Med., Volume 169, Number 4, February 2004, 518-524

A more recent version of this article appeared on February 15, 2004
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Submitted on May 15, 2003
Accepted on November 22, 2003

VENTILATION-INDUCED NEUTROPHIL INFILTRATION DEPENDS ON C-JUN N-TERMINAL KINASE

Li-Fu Li1, Lunyin Yu2, and Deborah A Quinn2*

1 Graduate Institute of Clinical Medical Sciences, Chang Gung University, Taoyuan, Taiwan; Pulmonary and Critical Care Units, Harvard Medical School and Massachusetts General Hospital, Boston, MA, USA, 2 Pulmonary and Critical Care Units, Harvard Medical School and Massachusetts General Hospital, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: dquinn1{at}partners.org.

Positive pressure ventilation with large tidal volumes has been shown to cause release of cytokines, including macrophage inflammatory protein-2, a functional equivalent of human Interleukin-8. The mechanisms regulating ventilation-induced cytokine production are unclear. Based on our previous in vitro model of lung cell stretch, we hypothesized that high tidal volume ventilation-induced macrophage inflammatory protein-2 production is dependent on the activation of the c-Jun N-terminal kinase. We exposed C57BL/6 mice to high tidal volume (30 ml/kg) or low tidal volume (6 ml/kg) mechanical ventilation for 5 hours. High tidal volume ventilation induced neutrophil migration into the lung, macrophage inflammatory protein-2 protein production, macrophage inflammatory protein-2 mRNA expression, and c-Jun N-terminal kinase activation. Large tidal volume ventilation of c-Jun N-terminal kinase knockout mice, and pharmacological c-Jun N-terminal kinase inhibition with SP600125 attenuated neutrophil sequestration, and blocked macrophage inflammatory protein-2 mRNA expression and macrophage inflammatory protein-2 production. We conclude that lung cell stretch in vivo, results in increased lung neutrophil sequestration and increased macrophage inflammatory protein-2 production, which was, at least in part, dependent, on the c-Jun N-terminal kinase pathway.
Key words: chemokine, mitogen-activated protein kinase, lung stretch




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