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Household mold exposure interacts with inflammation-related genetic variants on childhood asthma: a case–control study

BACKGROUND: A number of studies have examined the association between mold exposure and childhood asthma. However, the conclusions were inconsistent, which might be partly attributable to the lack of consideration of gene function, especially the key genes affecting the pathogenesis of childhood ast...

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Autores principales: Zhang, Yu, Hua, Li, Liu, Quan-Hua, Chu, Shu-Yuan, Gan, Yue-Xin, Wu, Min, Bao, Yi-Xiao, Chen, Qian, Zhang, Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8019181/
https://www.ncbi.nlm.nih.gov/pubmed/33810791
http://dx.doi.org/10.1186/s12890-021-01484-9
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author Zhang, Yu
Hua, Li
Liu, Quan-Hua
Chu, Shu-Yuan
Gan, Yue-Xin
Wu, Min
Bao, Yi-Xiao
Chen, Qian
Zhang, Jun
author_facet Zhang, Yu
Hua, Li
Liu, Quan-Hua
Chu, Shu-Yuan
Gan, Yue-Xin
Wu, Min
Bao, Yi-Xiao
Chen, Qian
Zhang, Jun
author_sort Zhang, Yu
collection PubMed
description BACKGROUND: A number of studies have examined the association between mold exposure and childhood asthma. However, the conclusions were inconsistent, which might be partly attributable to the lack of consideration of gene function, especially the key genes affecting the pathogenesis of childhood asthma. Research on the interactions between genes and mold exposure on childhood asthma is still very limited. We therefore examined whether there is an interaction between inflammation-related genes and mold exposure on childhood asthma. METHODS: A case–control study with 645 asthmatic children and 910 non-asthmatic children aged 3–12 years old was conducted. Eight single nucleotide polymorphisms (SNPs) in inflammation-related genes were genotyped using MassARRAY assay. Mold exposure was defined as self-reported visible mold on the walls. Associations between visible mold exposure, SNPs and childhood asthma were evaluated using logistic regression models. In addition, crossover analyses were used to estimate the gene-environment interactions on childhood asthma on an additive scale. RESULTS: After excluding children without information on visible mold exposure or SNPs, 608 asthmatic and 839 non-asthmatic children were included in the analyses. Visible mold exposure was reported in 151 asthmatic (24.8%) and 119 non-asthmatic children (14.2%) (aOR 2.19, 95% CI 1.62–2.97). The rs7216389 SNP in gasdermin B gene (GSDMB) increased the risk of childhood asthma with each C to T substitution in a dose-dependent pattern (additive model, aOR 1.32, 95% CI 1.11–1.57). Children carrying the rs7216389 T allele and exposed to visible mold dramatically increased the risk of childhood asthma (aOR 3.21; 95% CI 1.77–5.99). The attributable proportion due to the interaction (AP: 0.47, 95% CI 0.03–0.90) and the relative excess risk due to the interaction (RERI: 1.49, 95% CI 0–2.99) were statistically significant. CONCLUSIONS: In the present study, there was a significant additive interaction between visible mold exposure and rs7216389 SNP on childhood asthma. Future studies need to consider the gene-environment interactions when exploring the risk factors of childhood asthma. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12890-021-01484-9.
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spelling pubmed-80191812021-04-05 Household mold exposure interacts with inflammation-related genetic variants on childhood asthma: a case–control study Zhang, Yu Hua, Li Liu, Quan-Hua Chu, Shu-Yuan Gan, Yue-Xin Wu, Min Bao, Yi-Xiao Chen, Qian Zhang, Jun BMC Pulm Med Article BACKGROUND: A number of studies have examined the association between mold exposure and childhood asthma. However, the conclusions were inconsistent, which might be partly attributable to the lack of consideration of gene function, especially the key genes affecting the pathogenesis of childhood asthma. Research on the interactions between genes and mold exposure on childhood asthma is still very limited. We therefore examined whether there is an interaction between inflammation-related genes and mold exposure on childhood asthma. METHODS: A case–control study with 645 asthmatic children and 910 non-asthmatic children aged 3–12 years old was conducted. Eight single nucleotide polymorphisms (SNPs) in inflammation-related genes were genotyped using MassARRAY assay. Mold exposure was defined as self-reported visible mold on the walls. Associations between visible mold exposure, SNPs and childhood asthma were evaluated using logistic regression models. In addition, crossover analyses were used to estimate the gene-environment interactions on childhood asthma on an additive scale. RESULTS: After excluding children without information on visible mold exposure or SNPs, 608 asthmatic and 839 non-asthmatic children were included in the analyses. Visible mold exposure was reported in 151 asthmatic (24.8%) and 119 non-asthmatic children (14.2%) (aOR 2.19, 95% CI 1.62–2.97). The rs7216389 SNP in gasdermin B gene (GSDMB) increased the risk of childhood asthma with each C to T substitution in a dose-dependent pattern (additive model, aOR 1.32, 95% CI 1.11–1.57). Children carrying the rs7216389 T allele and exposed to visible mold dramatically increased the risk of childhood asthma (aOR 3.21; 95% CI 1.77–5.99). The attributable proportion due to the interaction (AP: 0.47, 95% CI 0.03–0.90) and the relative excess risk due to the interaction (RERI: 1.49, 95% CI 0–2.99) were statistically significant. CONCLUSIONS: In the present study, there was a significant additive interaction between visible mold exposure and rs7216389 SNP on childhood asthma. Future studies need to consider the gene-environment interactions when exploring the risk factors of childhood asthma. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12890-021-01484-9. BioMed Central 2021-04-02 /pmc/articles/PMC8019181/ /pubmed/33810791 http://dx.doi.org/10.1186/s12890-021-01484-9 Text en © The Author(s) 2021 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Article
Zhang, Yu
Hua, Li
Liu, Quan-Hua
Chu, Shu-Yuan
Gan, Yue-Xin
Wu, Min
Bao, Yi-Xiao
Chen, Qian
Zhang, Jun
Household mold exposure interacts with inflammation-related genetic variants on childhood asthma: a case–control study
title Household mold exposure interacts with inflammation-related genetic variants on childhood asthma: a case–control study
title_full Household mold exposure interacts with inflammation-related genetic variants on childhood asthma: a case–control study
title_fullStr Household mold exposure interacts with inflammation-related genetic variants on childhood asthma: a case–control study
title_full_unstemmed Household mold exposure interacts with inflammation-related genetic variants on childhood asthma: a case–control study
title_short Household mold exposure interacts with inflammation-related genetic variants on childhood asthma: a case–control study
title_sort household mold exposure interacts with inflammation-related genetic variants on childhood asthma: a case–control study
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8019181/
https://www.ncbi.nlm.nih.gov/pubmed/33810791
http://dx.doi.org/10.1186/s12890-021-01484-9
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