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B-INDUCING KINASES
1 Chang Gung University, Taiwan; Department of Medicine, Pulmonary and Critical Care and Renal Units, Massachusetts General Hospital, and Havard Medical School, Boston, MA, USA
2 Department of Medicine, Pulmonary and Critical Care and Renal Units, Massachusetts General Hospital, and Havard Medical School, Boston, MA, USA
3 Internal Medicine and Department of Nephrology, Amiens Hospital, France; Department of Medicine, Pulmonary and Critical Care and Renal Units, Massachusetts General Hospital, and Havard Medical School, Boston, MA, USA
4 Department of Medicine, Molecular Cardiology Research Institute, Tufts New England Medical Center, 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 Interleukin (IL)-8. The mechanisms regulating lung stretch-induced cytokine production are unclear. We hypothesized that stretch-induced IL-8 production is dependent on the activation of the mitogen-activated protein (MAP) kinases, c-Jun N-terminal kinases (JNK), p38 and/or extracellular signal-regulated kinase (ERK) 1/2. We exposed A549 cells, a type II-like alveolar epithelial cell line, to cyclic stretch at 20 cycles/minute for 5 minutes to two hours. Cyclic stretch induced IL-8 protein production, IL-8 mRNA expression and JNK activation, but only transient activation of p38 and ERK1/2. Inhibition of stretch-induced JNK activation by adenovirus-mediated gene transfer of SEK-1 (KR), a dominant inhibitory mutant of SEK-1, the immediate upstream activator of the JNKs, and pharmacological JNK inhibitor II SP600125, blocked IL-8 mRNA expression and attenuated IL-8 production. Inhibition of p38 and ERK1/2 did not affect stretch-induced IL-8 production. Stretch-induced activation NF-
B and AP-1 was blocked by NF-B inhibitor and JNK inhibitor, respectively. NF-IL-6 site was not essential for cyclic stretch-induced IL-8 promoter activity. Stretch also induced NF-B-inducing kinase (NIK) activation, and inhibition of NF-B attenuated IL-8 mRNA expression and IL-8 production. We conclude that stretch-induced transcriptional regulation of IL-8 mRNA and IL-8 production was via activation of AP-1 and NF-B and was dependent on JNK and NIK activation, respectively.
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