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Published ahead of print on August 27, 2004, doi:10.1165/rcmb.2004-0006OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 6, December 2004, 633-642

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Submitted on January 7, 2004
Revised on August 26, 2004

Cigarette smoke alters chromatin remodelling and induces pro-inflammatory genes in rat lungs

J. A Marwick1, P. A Kirkham2, C. S Stevenson2, H. Danahay2, J. Giddings2, K. Butler2, K. Donaldson1, W. MacNee1, and I. Rahman3*

1 Department of Respiratory Medicine, University of Edinburgh, Edinburgh, United Kingdom, 2 Novartis Institute for Biomedical Research, Horsham, United Kingdom, 3 Department of Environmental Medicine, Division of Lung Biology and Disease Program, University of Rochester Medical Center, Rochester, NY, USA

* To whom correspondence should be addressed. E-mail: Irfan_Rahman{at}urmc.rochester.edu.

Cigarette smoke-triggered inflammation is considered to play a central role in the development of chronic obstructive pulmonary disease (COPD) by a mechanism that may involve enhanced pro-inflammatory gene transcription. Histone acetylation and deacetylation is a key regulator of the specificity and duration of gene transcription. Disruption in the nuclear histone acetylation:deacetylation balance (chromatin remodelling) may result in excessive transcription of specific pro-inflammatory genes in the lungs. In this study we show that cigarette smoke exposure results in an influx of inflammatory cells and chromatin modifications in rat lungs. This was associated with an increase in the active phosphorylated form of p38 MAPK concomitant with increased histone 3 phospho-acetylation, histone 4 acetylation and increased DNA binding of the redox-sensitive transcription factors NF-{kappa}B, independent of inhibitory protein-kappaB (I{kappa}B) degradation, and activator protein 1 (AP-1). We also observed decreased histone deacetylase 2 (HDAC2) activity, which is due to protein modification by aldehydes and nitric oxide products present in cigarette smoke. Furthermore, we show that corticosteroid treatment has no effect on smoke-induced pro-inflammatory mediator release. These findings suggest a possible molecular mechanism by which cigarette smoke drives pro-inflammatory gene transcription and an inflammatory response in the lungs.




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