- Meeting abstract
- Open Access
Tobacco smoke induces changes in IL-1 family in bronchial epithelial cells obtained from asthmatic individuals
© Gagné-Ouellet et al; licensee BioMed Central Ltd. 2014
Published: 18 December 2014
Exposure to tobacco smoke (ETS) induces epigenetic modifications including DNA methylation . In asthma, it has been shown that those modifications affect immune cell differentiation by downregulating expression of specific pro-inflammatory cytokines [2–4]. Interleukin 1 (IL-1) is recognized to be increased in asthma  and by cigarette smoke [5, 6]. Based on previous genetic association [7, 8] and DNA methylation signature of receptors in asthma and/or atopy the aim of this study is to evaluate the changes in expression and methylation pattern induced by ETS for IL-1 subunit alpha (IL-1A) and beta (IL-1B), receptors type I (IL-1R1), type II (IL-1R2) and antagonist (IL-1RA) and for interleukin 33 (IL-33) in lung tissue.
Primary epithelium cells isolated from bronchial biopsies of mild asthmatics and non-asthmatics individuals were exposed to whole tobacco smoke according to method described . Level of mRNA was measured by qRT-PCR and methylation was assessed by bis-pyrosequencing for IL-1A, IL-1B, IL-1R1, IL-1R2, IL-1RA and IL-33.
ETS increased mRNA level of IL-1A and IL-1B in both asthmatic and non-asthmatic individuals. IL-33 showed a significant decrease in gene expression following ETS in asthmatic individuals but not in non-asthmatics. IL-1R1 was decreased in non-asthmatic individuals but no change was observed in asthmatics. IL-1R2 and IL-1RA increased in both asthmatic and non-asthmatic individuals. We observed DNA methylation differences in IL-1R1 promoter between ETS and non-ETS cells.
Modifications of genes expression induced by tobacco smoke could modify IL-1 family resulting in an increase of inflammation in lung tissues of asthmatic and non-asthmatic individuals. These changes may be induced by DNA methylation. Efforts to better interpret and integrate data from genetics and epigenetics are needed to better understand the biology of asthma as well as a better comprehension of the impact of tobacco smoke in the inflammatory component of asthma.
- Wilhelm-Benartzi CS: Association of secondhand smoke exposures with DNA methylation in bladder carcinomas. Cancer causes & control : CCC. 2011, 22 (8): 1205-13. 10.1007/s10552-011-9788-6.PubMed CentralView ArticlePubMedGoogle Scholar
- Lange P: A 15-year follow-up study of ventilatory function in adults with asthma. The New England journal of medicine. 1998, 339 (17): 1194-200. 10.1056/NEJM199810223391703.View ArticlePubMedGoogle Scholar
- White GP: CpG methylation patterns in the IFNgamma promoter in naive T cells: variations during Th1 and Th2 differentiation and between atopics and non-atopics. Pediatric Allergy and Immunology: official publication of the European Society of Pediatric Allergy and Immunology. 2006, 17 (8): 557-64. 10.1111/j.1399-3038.2006.00465.x.View ArticleGoogle Scholar
- Jones B, Chen J: Inhibition of IFN-gamma transcription by site-specific methylation during T helper cell development. The EMBO Journal. 2006, 25 (11): 2443-52. 10.1038/sj.emboj.7601148.PubMed CentralView ArticlePubMedGoogle Scholar
- Dinarello CA: Biologic basis for interleukin-1 in disease. Blood. 1996, 87 (6): 2095-2147.PubMedGoogle Scholar
- Fu JJ: Systemic inflammation is associated with differential gene expression and airway neutrophilia in asthma. Omics: A Journal of Jntegrative Biology. 2013, 17 (4): 187-199. 10.1089/omi.2012.0104.View ArticleGoogle Scholar
- Daley D: Analyses of associations with asthma in four asthma population samples from Canada and Australia. Human Genetics. 2009, 125 (4): 445-459. 10.1007/s00439-009-0643-8.View ArticlePubMedGoogle Scholar
- Daley D: Associations and interactions of genetic polymorphisms in innate immunity genes with early viral infections and susceptibility to asthma and asthma-related phenotypes. The Journal of Allergy and Clinical Immunology. 2012, 130 (6): 1284-1293. 10.1016/j.jaci.2012.07.051.View ArticlePubMedGoogle Scholar
- Semlali A: Whole cigarette smoke promotes human gingival epithelial cell apoptosis and inhibits cell repair processes. Journal of Periodontal Pesearch. 2011, 46 (5): 533-541.Google Scholar
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.