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Published ahead of print on April 21, 2005, doi:10.1165/rcmb.2005-0022OC

Am. J. Respir. Cell Mol. Biol., Volume 33, Number 1, July 2005, 97-104

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Submitted on January 12, 2005
Revised on April 20, 2005

IL-17 Induces Hyperresponsive IL-8 and IL-6 Production to TNF-{alpha} in Structural Lung Cells

Arjen van den Berg1*, Mathys Kuiper2, Mieke Snoek1, Wim Timens3, Dirkje S Postma4, Henk M Jansen2, and Rene Lutter1

1 Department of Pulmonology, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands; Laboratory of Experimental Immunology, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands, 2 Department of Pulmonology, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands, 3 Department of Pathology, University of Groningen, Groningen, The Netherlands, 4 Department of Pulmonology, University of Groningen, Groningen, The Netherlands

* To whom correspondence should be addressed. E-mail: a.vandenberg{at}amc.uva.nl.

Lung epithelial cells contribute to local inflammation by the production of pro-inflammatory mediators like IL-8 and IL-6. Although their production depends on gene transcription, previous studies showed that post-transcriptional mechanisms modulate IL-8 and IL-6 production. Human lung epithelial cells turn from normoresponsive into hyperresponsive IL-8- and IL-6-producing cells when their IL-8 and IL-6 mRNA degradation is reduced. We hypothesized that IL-17, a mediator predominantly released by memory T cells and present in airways of asthmatics, would modulate rather than induce IL-8 and IL-6 production by both human lung epithelial cells and fibroblasts. We here show for both cell types that IL-17 was a weak stimulus of IL-8 and IL-6 production, but markedly enhanced IL-8 and IL-6 responses to another stimulus, such as TNF-{alpha}. This modulatory effect of IL-17 was paralleled by a reduced IL-8 and IL-6 mRNA degradation, with no effect on IL-8 and IL-6 gene transcription. In conclusion, IL-17 particularly affects post-transcriptional regulation of IL-8 and IL-6 expression leading to enhanced IL-8 and IL-6 responses to secondary stimuli, and is only a weak pro-inflammatory stimulus by itself. This poses the interesting concept that by releasing IL-17 from memory T cells, the adaptive immune system instructs lung structural cells as part of the innate immune system to respond more vigorously.




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