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      Atopic asthma after rhinovirus‐induced wheezing is associated with DNA methylation change in the SMAD3 gene promoter

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          Abstract

          Children with rhinovirus‐induced severe early wheezing have an increased risk of developing asthma later in life. The exact molecular mechanisms for this association are still mostly unknown. To identify potential changes in the transcriptional and epigenetic regulation in rhinovirus‐associated atopic or nonatopic asthma, we analyzed a cohort of 5‐year‐old children (n = 45) according to the virus etiology of the first severe wheezing episode at the mean age of 13 months and to 5‐year asthma outcome. The development of atopic asthma in children with early rhinovirus‐induced wheezing was associated with DNA methylation changes at several genomic sites in chromosomal regions previously linked to asthma. The strongest changes in atopic asthma were detected in the promoter region of SMAD3 gene at chr 15q22.33 and introns of DDO/ METTL24 genes at 6q21. These changes were validated to be present also at the average age of 8 years.

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          Controlling the False Discovery Rate: A Practical and Powerful Approach to Multiple Testing

          Yoav Benjamini, Yosef Hochberg (1995)
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            Wheezing rhinovirus illnesses in early life predict asthma development in high-risk children.

            Daniel J. Jackson, Ronald Gangnon, Michael D C Evans … (2008)
            Virus-induced wheezing episodes in infancy often precede the development of asthma. Whether infections with specific viral pathogens confer differential future asthma risk is incompletely understood. To define the relationship between specific viral illnesses and early childhood asthma development. A total of 259 children were followed prospectively from birth to 6 years of age. The etiology and timing of specific viral wheezing respiratory illnesses during early childhood were assessed using nasal lavage, culture, and multiplex reverse transcriptase-polymerase chain reaction. The relationships of these virus-specific wheezing illnesses and other risk factors to the development of asthma were analyzed. Viral etiologies were identified in 90% of wheezing illnesses. From birth to age 3 years, wheezing with respiratory syncytial virus (RSV) (odds ratio [OR], 2.6), rhinovirus (RV) (OR, 9.8), or both RV and RSV (OR , 10) was associated with increased asthma risk at age 6 years. In Year 1, both RV wheezing (OR, 2.8) and aeroallergen sensitization (OR, 3.6) independently increased asthma risk at age 6 years. By age 3 years, wheezing with RV (OR, 25.6) was more strongly associated with asthma at age 6 years than aeroallergen sensitization (OR, 3.4). Nearly 90% (26 of 30) of children who wheezed with RV in Year 3 had asthma at 6 years of age. Among outpatient viral wheezing illnesses in infancy and early childhood, those caused by RV infections are the most significant predictors of the subsequent development of asthma at age 6 years in a high-risk birth cohort.
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              Innate and adaptive immune responses in asthma.

              Stephen T. Holgate (2012)
              The recognition that asthma is primarily an inflammatory disorder of the airways associated with T helper type 2 (T(H)2) cell-dependent promotion of IgE production and recruitment of mast cells and eosinophils has provided the rationale for disease control using inhaled corticosteroids and other anti-inflammatory drugs. As more has been discovered about the cytokine, chemokine and inflammatory pathways that are associated with T(H)2-driven adaptive immunity, attempts have been made to selectively inhibit these in the hope of discovering new therapeutics as predicted from animal models of allergic inflammation. The limited success of this approach, together with the recognition that asthma is more than allergic inflammation, has drawn attention to the innate immune response in this disease. Recent advances in our understanding of the sentinel role played by innate immunity provides new targets for disease prevention and treatment. These include pathways of innate stimulation by environmental or endogenous pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) to influence the activation and trafficking of DCs, innate sources of cytokines, and the identification of new T cell subsets and lymphoid cells.
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                Author and article information

                Contributors
                R. J. Lund:
                ORCID: http://orcid.org/0000-0002-1068-5918
                riikka.lund@utu.fi
                Journal
                Journal ID (nlm-ta): Allergy
                Journal ID (iso-abbrev): Allergy
                Journal ID (doi): 10.1111/(ISSN)1398-9995
                Journal ID (publisher-id): ALL
                Title: Allergy
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 0105-4538
                ISSN (Electronic): 1398-9995
                Publication date (Electronic): 21 May 2018
                Publication date (Print): August 2018
                Volume: 73
                Issue: 8 ( doiID: 10.1111/all.2018.73.issue-8 )
                Pages: 1735-1740
                Affiliations
                [ 1 ] Turku Centre for Biotechnology University of Turku and Åbo Akademi University Turku Finland
                [ 2 ] Department of Information and Computer Science Aalto University Helsinki Finland
                [ 3 ] Department of Paediatrics and Adolescent Medicine Turku University Hospital University of Turku Turku Finland
                [ 4 ] Research Centre of Applied and Preventive Cardiovascular Medicine University of Turku Turku Finland
                [ 5 ] Department of Virology University of Turku Turku Finland
                [ 6 ] Department of Clinical Virology Turku University Hospital Turku Finland
                [ 7 ] Swiss Institute of Allergy and Asthma Research (SIAF) Christine Kühne‐Center for Allergy Research and Education (CK‐CARE) University of Zürich Davos Switzerland
                Author notes
                [*] [* ] Correspondence

                Riikka Lund, Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland.

                Email: riikka.lund@ 123456utu.fi

                Author information
                http://orcid.org/0000-0002-1068-5918
                http://orcid.org/0000-0002-2828-7483
                http://orcid.org/0000-0003-2748-5362
                Article
                Publisher ID: ALL13473
                DOI: 10.1111/all.13473
                PMC ID: 6055882
                PubMed ID: 29729188
                SO-VID: 7733aceb-b948-4702-8ca7-0d0079df99a2
                Copyright © © 2018 The Authors. Allergy Published by John Wiley & Sons Ltd.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                Date accepted : 27 April 2018
                Page count
                Figures: 1, Tables: 1, Pages: 6, Words: 3710
                Funding
                Funded by: Academy of Finland
                Award ID: 114034
                Award ID: 132595
                Award ID: 267133
                Funded by: Academy of Finland the Centre of Excellence in Molecular Systems Immunology and Physiology Research
                Funded by: Sigrid Juselius Foundation
                Funded by: Foundation for Pediatric Research
                Categories
                Subject: Brief Communication
                Subject: Brief Communication
                Custom metadata
                source-schema-version-number 2.0
                component-id all13473
                cover-date August 2018
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.4.3 mode:remove_FC converted:23.07.2018

                ScienceOpen disciplines: Immunology
                Keywords: asthma,epigenome,rhinovirus,transcriptome,wheezing
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: asthma, epigenome, rhinovirus, transcriptome, wheezing

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