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Nat Commun. 2019 Jul 12;10(1):3095. doi: 10.1038/s41467-019-11058-3.

The nasal methylome as a biomarker of asthma and airway inflammation in children.

Author information

1
Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, Berkeley, CA, 94720, USA. andres.cardenas@berkeley.edu.
2
Department of Population Medicine, Division of Chronic Disease Research Across the Lifecourse, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, MA, 02215, USA. andres.cardenas@berkeley.edu.
3
Department of Population Medicine, Division of Chronic Disease Research Across the Lifecourse, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, MA, 02215, USA.
4
Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA, 02115, USA.
5
Diabetes Unit, Massachusetts General Hospital, Boston, 02114, MA, USA.
6
Massachusetts General Hospital, Pulmonary/Critical Care, Boston, MA, 02114, USA.
7
Division of Pediatric Pulmonary Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, 15224, USA.
8
Division of Pediatric Pulmonary Medicine, University of Rochester Medical Center, Rochester, NY, 14642, USA.
9
Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, NY, 10032, USA.
10
Department of Medicine, Brigham and Women's Hospital, Channing Division of Network Medicine, Harvard Medical School, Boston, MA, 02115, USA.
11
Department of Environmental Health, Harvard T. H. Chan School of Public Health, Boston, MA, 02115, USA.

Abstract

The nasal cellular epigenome may serve as biomarker of airway disease and environmental response. Here we collect nasal swabs from the anterior nares of 547 children (mean-age 12.9 y), and measure DNA methylation (DNAm) with the Infinium MethylationEPIC BeadChip. We perform nasal Epigenome-Wide Association analyses (EWAS) of current asthma, allergen sensitization, allergic rhinitis, fractional exhaled nitric oxide (FeNO) and lung function. We find multiple differentially methylated CpGs (FDR < 0.05) and Regions (DMRs; ≥ 5-CpGs and FDR < 0.05) for asthma (285-CpGs), FeNO (8,372-CpGs; 191-DMRs), total IgE (3-CpGs; 3-DMRs), environment IgE (17-CpGs; 4-DMRs), allergic asthma (1,235-CpGs; 7-DMRs) and bronchodilator response (130-CpGs). Discovered DMRs annotated to genes implicated in allergic asthma, Th2 activation and eosinophilia (EPX, IL4, IL13) and genes previously associated with asthma and IgE in EWAS of blood (ACOT7, SLC25A25). Asthma, IgE and FeNO were associated with nasal epigenetic age acceleration. The nasal epigenome is a sensitive biomarker of asthma, allergy and airway inflammation.

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