Imperial College London

DrElaineFuertes

Faculty of MedicineNational Heart & Lung Institute

Imperial College Junior Research Fellow
 
 
 
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Contact

 

+44 (0)20 7594 7939e.fuertes

 
 
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Location

 

Emmanuel Kaye BuildingRoyal Brompton Campus

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Summary

 

Publications

Citation

BibTex format

@article{Hüls:2018:10.1111/pai.12903,
author = {Hüls, A and Klümper, C and MacIntyre, EA and Brauer, M and Melén, E and Bauer, M and Berdel, D and Bergström, A and Brunekreef, B and Chan-Yeung, M and Fuertes, E and Gehring, U and Gref, A and Heinrich, J and Standl, M and Lehmann, I and Kerkhof, M and Koppelman, GH and Kozyrskyj, AL and Pershagen, G and Carlsten, C and Krämer, U and Schikowski, T and TAG, Study Group},
doi = {10.1111/pai.12903},
journal = {Pediatric Allergy and Immunology},
pages = {596--605},
title = {Atopic dermatitis: Interaction between genetic variants of GSTP1, TNF, TLR2 & TLR4 and air pollution in early life},
url = {http://dx.doi.org/10.1111/pai.12903},
volume = {29},
year = {2018}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - BACKGROUND: Associations between traffic-related air pollution (TRAP) and childhood atopic dermatitis (AD) remain inconsistent, possibly due to unexplored gene-environment interactions. The aim of this study was to examine whether a potential effect of TRAP on AD prevalence in children is modified by selected single nucleotide polymorphisms (SNPs) related to oxidative stress and inflammation. METHODS: Doctor-diagnosed AD up to age 2 years and at 7-8 years, as well as AD symptoms up to age 2 years, were assessed using parental-reported questionnaires in six birth cohorts (N=5,685). Associations of nitrogen dioxide (NO2) estimated at the home address of each child at birth, and nine SNPs within the GSTP1, TNF, TLR2, or TLR4 genes with AD were examined. Weighted genetic risk scores (GRS) were calculated from the above SNPs and used to estimate combined marginal genetic effects of oxidative stress and inflammation on AD and its interaction with TRAP. RESULTS: GRS was associated with childhood AD and modified the association between NO2 and doctor-diagnosed AD up to the age of 2 years (p(interaction)=0.029). This interaction was mainly driven by a higher susceptibility to air pollution in TNF rs1800629 minor allele (A) carriers. TRAP was not associated with the prevalence of AD in the general population. CONCLUSIONS: The marginal genetic association of a weighted GRS from GSTP1, TNF, TLR2, and TLR4 SNPs and its interaction with air pollution supports the role of oxidative stress & inflammation in AD. This article is protected by copyright. All rights reserved.
AU - Hüls,A
AU - Klümper,C
AU - MacIntyre,EA
AU - Brauer,M
AU - Melén,E
AU - Bauer,M
AU - Berdel,D
AU - Bergström,A
AU - Brunekreef,B
AU - Chan-Yeung,M
AU - Fuertes,E
AU - Gehring,U
AU - Gref,A
AU - Heinrich,J
AU - Standl,M
AU - Lehmann,I
AU - Kerkhof,M
AU - Koppelman,GH
AU - Kozyrskyj,AL
AU - Pershagen,G
AU - Carlsten,C
AU - Krämer,U
AU - Schikowski,T
AU - TAG,Study Group
DO - 10.1111/pai.12903
EP - 605
PY - 2018///
SN - 1399-3038
SP - 596
TI - Atopic dermatitis: Interaction between genetic variants of GSTP1, TNF, TLR2 & TLR4 and air pollution in early life
T2 - Pediatric Allergy and Immunology
UR - http://dx.doi.org/10.1111/pai.12903
UR - https://www.ncbi.nlm.nih.gov/pubmed/29624745
UR - http://hdl.handle.net/10044/1/59032
VL - 29
ER -