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Am J Physiol Lung Cell Mol Physiol 283: L690-L699, 2002. First published March 15, 2002; doi:10.1152/ajplung.00060.2002
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Vol. 283, Issue 4, L690-L699, October 2002

EDITORIAL FOCUS
Regulation of human airway epithelial cell IL-8 expression by MAP kinases

Jing Li1,*, Sreedharan Kartha1,*, Svetlana Iasvovskaia1, Alan Tan1, Rajesh K. Bhat1, Joel M. Manaligod1, Kristen Page1, Allan R. Brasier2, and Marc B. Hershenson1

1 Department of Pediatrics, University of Chicago, Chicago, Illinois 60637; and 2 Department of Medicine, University of Texas Medical Branch, Galveston, Texas 77555-1060

Recent studies indicate that maximal IL-8 protein expression requires activation of NF-kappa B as well as activation of the MAP kinases ERK, JNK, and p38. However, the precise relationship between NF-kappa B transactivation and MAP kinase activation remains unclear. We examined the requirements of NF-kappa B, ERK, JNK, and p38 for TNF-alpha -induced transcription from the IL-8 promoter in a human bronchial epithelial cell line. Treatment with TNF-alpha induced activation of all three MAP kinases. Using a combination of chemical and dominant-negative inhibitors, we found that inhibition of NF-kappa B, ERK, and JNK, but not p38, each decreased TNF-alpha -induced transcription from the IL-8 promoter. Inhibition of JNK signaling also substantially reduced TNF-alpha -induced NF-kappa B transactivation, whereas inhibition of ERK and p38 had no effect. On the other hand, ERK was required and sufficient for TNF-alpha -induced activation of activator protein (AP)-1 promoter sequences, which together function as a basal level enhancer. JNK activation was also required for AP-1 transactivation. Finally, inhibition of p38 attenuated IL-8 protein abundance, suggesting that p38 regulates IL-8 expression in a posttranscriptional manner. We conclude that, in human airway epithelial cells, MAP kinases may regulate IL-8 promoter activity by NF-kappa B-dependent (in the case of JNK) and -independent (ERK) processes, as well as by posttranscriptional mechanisms (p38).

cytokines; inflammation; signal transduction; transcription factors; interleukin 8; mitogen-activated protein

* J. Li and S. Kartha contributed equally to this work.




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