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Gene, Environment and Allergic Diseases

A special issue of International Journal of Environmental Research and Public Health (ISSN 1660-4601). This special issue belongs to the section "Global Health".

Deadline for manuscript submissions: closed (31 January 2020) | Viewed by 4512

Special Issue Editor


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Guest Editor
1. Department of Pediatrics, Taipei Hospital, Ministry of Health and Welfare, Taipei 11267, Taiwan
2. School of Medicine, National Yang Ming Chiao Tung University, Taipei 112, Taiwan
3. College of Public Health, China Medical University, Taichung 40402, Taiwan
4. National Institute of Environmental Health Sciences, National Health Research Institutes, Miaoli 35053, Taiwan
Interests: probiotics, microbiome; genetic epidemiology; environmental epigenetics; pediatric environmental health; allergic diseases
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Special Issue Information

Dear Colleagues,

We are organizing a Special Issue on “Gene, Environment, and Allergic Diseases” that will be published in the International Journal of Environmental Research and Public Health (IJERPH, IF 2.145, ISSN 1660-4601).  The venue is a peer-reviewed scientific journal that publishes articles and communications in the interdisciplinary area of environmental health and public health. For detailed information on the journal, we refer you to https://0-www-mdpi-com.brum.beds.ac.uk/journal/ijerph/special_issues/Dermatitis. To check suitability, we encourage authors to send a short abstract or tentative title in advance to the Editorial Office at: [email protected]

The prevalence of allergic diseases increased dramatically over the past decade. It is generally believed that such rapid increase can be explained by the complex interplay of genetic and environmental factors. Environmental exposures, such as allergens, tobacco smoke, air pollutants, endocrine disruptors, microbes, medication, diet, and stress may have important effects on allergic diseases. On the basis of how rapidly environmental changes have affected the incidence of allergic diseases, a full understanding of gene–environment interactions requires that epigenetic mechanisms and classical genetic mechanisms be taken into account. Insights into the relationship between genetic, epigenetic, and environmental factors may pave the way for targeted therapies for allergic diseases in the era of personalized medicine and prevent the atopic march. 

With this Special Issue, we invite you to submit high-quality original research articles or reviews that provide solid new findings extending the current state of knowledge on allergic disease spread. Preference will be given to contributions using longitudinal data and or experimental/intervention designs. All manuscripts will be peer-reviewed by experts in the field and are due no later than the end of January 2020. IJERPH is fully open access. Open access (unlimited and free access by readers) increases publicity and promotes more frequent citations, as indicated by several studies. For further details on the submission process, please see the instructions for authors on the journal website.

Kind regards,

Dr. I-Jen Wang
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Environmental Research and Public Health is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2500 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Allergic diseases (atopic dermatitis, allergic rhinitis, asthma)
  • Gene
  • Epigenetics
  • Biomarkers
  • Exposures
  • Probiotics

Published Papers (1 paper)

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Research

13 pages, 1685 KiB  
Article
Bisphenol a Exposure, DNA Methylation, and Asthma in Children
by Chia-Feng Yang, Wilfried J. J. Karmaus, Chen-Chang Yang, Mei-Lien Chen and I-Jen Wang
Int. J. Environ. Res. Public Health 2020, 17(1), 298; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph17010298 - 01 Jan 2020
Cited by 29 | Viewed by 4228
Abstract
Epidemiological studies have reported the relationship between bisphenol A (BPA) exposure and increased prevalence of asthma, but the mechanisms remain unclear. Here, we investigated whether BPA exposure and DNA methylation related to asthma in children. We collected urinary and blood samples from 228 [...] Read more.
Epidemiological studies have reported the relationship between bisphenol A (BPA) exposure and increased prevalence of asthma, but the mechanisms remain unclear. Here, we investigated whether BPA exposure and DNA methylation related to asthma in children. We collected urinary and blood samples from 228 children (Childhood Environment and Allergic Diseases Study cohort) aged 3 years. Thirty-three candidate genes potentially interacting with BPA exposure were selected from a toxicogenomics database. DNA methylation was measured in 22 blood samples with top-high and bottom-low exposures of BPA. Candidate genes with differential methylation levels were validated by qPCR and promoter associated CpG islands have been investigated. Correlations between the methylation percentage and BPA exposure and asthma were analyzed. According to our findings, MAPK1 showed differential methylation and was further investigated in 228 children. Adjusting for confounders, urinary BPA glucuronide (BPAG) level inversely correlated with MAPK1 promoter methylation (β = −0.539, p = 0.010). For the logistic regression analysis, MAPK1 methylation status was dichotomized into higher methylated and lower methylated groups with cut off continuous variable of median of promoter methylation percentage (50%) while performing the analysis. MAPK1 methylation was lower in children with asthma than in children without asthma (mean ± SD; 69.82 ± 5.88% vs. 79.82 ± 5.56%) (p = 0.001). Mediation analysis suggested that MAPK1 methylation acts as a mediation variable between BPA exposure and asthma. The mechanism of BPA exposure on childhood asthma might, therefore, be through the alteration of MAPK1 methylation. The mechanism of BPA exposure on childhood asthma might, therefore, be through the alteration of MAPK1 methylation. Full article
(This article belongs to the Special Issue Gene, Environment and Allergic Diseases)
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