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Tobacco smoke induces changes in IL-1 family in bronchial epithelial cells obtained from asthmatic individuals

Background

Exposure to tobacco smoke (ETS) induces epigenetic modifications including DNA methylation [1]. In asthma, it has been shown that those modifications affect immune cell differentiation by downregulating expression of specific pro-inflammatory cytokines [24]. Interleukin 1 (IL-1) is recognized to be increased in asthma [5] 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.

Methods

Primary epithelium cells isolated from bronchial biopsies of mild asthmatics and non-asthmatics individuals were exposed to whole tobacco smoke according to method described [9]. 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.

Results

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.

Conclusions

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.

References

  1. 1.

    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 Central  Article  PubMed  Google Scholar 

  2. 2.

    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.

    CAS  Article  PubMed  Google Scholar 

  3. 3.

    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.

    Article  Google Scholar 

  4. 4.

    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 Central  CAS  Article  PubMed  Google Scholar 

  5. 5.

    Dinarello CA: Biologic basis for interleukin-1 in disease. Blood. 1996, 87 (6): 2095-2147.

    CAS  PubMed  Google Scholar 

  6. 6.

    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.

    CAS  Article  Google Scholar 

  7. 7.

    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.

    Article  PubMed  Google Scholar 

  8. 8.

    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.

    CAS  Article  PubMed  Google Scholar 

  9. 9.

    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.

    CAS  Google Scholar 

Download references

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Correspondence to Valérie Gagné-Ouellet.

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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.

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Gagné-Ouellet, V., Jacques, É., Boucher-Lafleur, AM. et al. Tobacco smoke induces changes in IL-1 family in bronchial epithelial cells obtained from asthmatic individuals. All Asth Clin Immun 10, A55 (2014). https://doi.org/10.1186/1710-1492-10-S2-A55

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Keywords

  • Asthma
  • Lung Tissue
  • Tobacco Smoke
  • Bronchial Epithelial Cell
  • Mild Asthmatic