Immunologic Research

, Volume 58, Issue 2, pp 369–373

Polycyclic aromatic hydrocarbons, tobacco smoke, and epigenetic remodeling in asthma

Authors

    • Division of Allergy and ImmunologyStanford University School of Medicine
  • K. M. Hew
    • Division of Allergy and ImmunologyStanford University School of Medicine
  • U. C. Nygaard
    • Division of Allergy and ImmunologyStanford University School of Medicine
    • Division of Environmental MedicineNorwegian Institute of Public Health
  • K. C. Nadeau
    • Division of Allergy and ImmunologyStanford University School of Medicine
IMMUNOLOGY AT STANFORD UNIVERSITY

DOI: 10.1007/s12026-014-8508-1

Cite this article as:
Klingbeil, E.C., Hew, K.M., Nygaard, U.C. et al. Immunol Res (2014) 58: 369. doi:10.1007/s12026-014-8508-1

Abstract

Environmental determinants including aerosolized pollutants such as polycyclic aromatic hydrocarbons (PAHs) and tobacco smoke have been associated with exacerbation and increased incidence of asthma. The influence of aerosolized pollutants on the development of immune dysfunction in asthmatics has been suggested to be mediated through epigenetic remodeling. Genome accessibility and transcription are regulated primarily through DNA methylation, histone modification, and microRNA transcript silencing. Epigenetic remodeling has been shown in studies to be associated with Th2 polarization and associated cytokine and chemokine regulation in the development of asthma. This review will present evidence for the contribution of the aerosolized pollutants PAH and environmental tobacco smoke to epigenetic remodeling in asthma.

Keywords

AsthmaPolycyclic aromatic hydrocarbonsDiesel exhaust particlesEnvironmental tobacco smokeEpigenetic remodeling

Copyright information

© Springer Science+Business Media New York 2014