Polycyclic aromatic hydrocarbons, tobacco smoke, and epigenetic remodeling in asthma.
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.
Division of Allergy and Immunology, Stanford University School of Medicine, 300 Pasteur Drive, Rm. S-303, Stanford, CA, 94305-5107, USA, ekling@stanford.edu.
E C
EC
Klingbeil
K M
KM
Hew
U C
UC
Nygaard
K C
KC
Nadeau
D000818:Animals; D001249:Asthma / Q000209:etiology*; D044127:Epigenesis, Genetic; D005260:Female; D006801:Humans; D018811:Maternal Exposure / Q000009:adverse effects; D011084:Polycyclic Aromatic Hydrocarbons / Q000009:adverse effects*; D011247:Pregnancy
D011084:Polycyclic Aromatic Hydrocarbons