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Atopic dermatitis: Interaction between genetic variants of GSTP 1 , TNF , TLR 2 , and TLR 4 and air pollution in early life
Author(s) -
Hüls Anke,
Klümper Claudia,
MacIntyre Elaina A.,
Brauer Michael,
Melén Erik,
Bauer Mario,
Berdel Dietrich,
Bergström Anna,
Brunekreef Bert,
ChanYeung Moira,
Fuertes Elaine,
Gehring Ulrike,
Gref Anna,
Heinrich Joachim,
Standl Marie,
Lehmann Irina,
Kerkhof Marjan,
Koppelman Gerard H.,
Kozyrskyj Anita L.,
Pershagen Göran,
Carlsten Christopher,
Krämer Ursula,
Schikowski Tamara
Publication year - 2018
Publication title -
pediatric allergy and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.269
H-Index - 89
eISSN - 1399-3038
pISSN - 0905-6157
DOI - 10.1111/pai.12903
Subject(s) - single nucleotide polymorphism , medicine , atopic dermatitis , immunology , snp , oxidative stress , allele , inflammation , population , genetics , genotype , gene , biology , environmental health
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 ( SNP s) 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, was assessed using parental‐reported questionnaires in six birth cohorts (N = 5685). Associations of nitrogen dioxide ( NO 2 ) estimated at the home address of each child at birth and nine SNP s within the GSTP 1 , TNF , TLR 2 , or TLR 4 genes with AD were examined. Weighted genetic risk scores ( GRS ) were calculated from the above SNP s 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 NO 2 and doctor‐diagnosed AD up to the age of 2 years ( P (interaction) = .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 GSTP 1 , TNF , TLR 2 , and TLR 4 SNP s and its interaction with air pollution supports the role of oxidative stress and inflammation in AD .