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Meta-Analysis
. 2020 Oct 21;21(1):55.
doi: 10.1186/s12865-020-00384-7.

Interleukin 4 gene polymorphism (-589C/T) and the risk of asthma: a meta-analysis and met-regression based on 55 studies

Affiliations
Meta-Analysis

Interleukin 4 gene polymorphism (-589C/T) and the risk of asthma: a meta-analysis and met-regression based on 55 studies

Ahmad Kousha et al. BMC Immunol. .

Abstract

Background: Numerous investigations have previously evaluated the association of interleukin (IL) 4 gene polymorphisms and the risk of asthma, conferring inconsistent results. To resolve the incongruent outcomes yielded from different single studies, we conducted the most up-to-date meta-analysis of IL4 gene -589C/T (rs2243250) polymorphism and susceptibility to asthma.

Methods: A systematic literature search was performed in ISI web of science, Scopus, Medline/PubMed databases prior to September 2020, and the pooled odds ratio (OR) and their corresponding 95% CI were calculated to determine the association strength.

Results: Literature search led to retrieving of 49 publications (55 case-control studies) containing 9572 cases and 9881 controls. It was revealed that IL4 gene -589C/T polymorphism increased the risk of asthma across all genetic models, including dominant model (OR = 1.22), recessive model (OR = 1.17), allelic model (OR = 1.21), and TT vs. CC model (OR = 1.34), but not the CT vs. TT model. The subgroup analysis by age indicated that IL4 gene -589C/T polymorphism was significantly associated with asthma risk in both pediatrics and adults. Additionally, the subgroup analysis by ethnicity revealed significant association in Asian, American, and Europeans. Finally, subgroup analysis by East Asian and non-East Asian populations indicated significant associations.

Conclusions: The current meta-analysis revealed that IL4 gene -589C/T polymorphism was a susceptibility risk in both pediatrics and adults in the whole and different ethnic groups.

Keywords: Asthma; Genetic susceptibility; Interleukin 4; Meta-analysis; Polymorphism.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Flow diagram of study selection process
Fig. 2
Fig. 2
Pooled OR and 95% CI of individual studies and pooled data for the association between Il-4 C589T polymorphism and asthma risk in; a allelic model, b recessive Model
Fig. 3
Fig. 3
Pooled odds ratio and 95% confidence interval of individual studies and pooled data for the association between IL-4 C589T polymorphism and asthma risk in different subgroups for; a dominant model [age subgroup], b dominant model [continent]
Fig. 4
Fig. 4
Pooled odds ratio and 95% confidence interval of individual studies and pooled data for the association between IL-4 C589T polymorphism and asthma risk in different subgroups for; a dominant model [East and non-East Asian], b dominant model [ethnicity]
Fig. 5
Fig. 5
Meta-regression plots of the association between IL-4 C589T polymorphism and risk of asthma based on; a Continent (dominant), b Genotyping methods (recessive), c Publication year (Allelic)
Fig. 6
Fig. 6
Begg’s funnel plot for publication bias test. Dominant model C598T. Each point represents a separate study for the indicated association
Fig. 7
Fig. 7
Sensitivity analysis in present meta-analysis investigates the single nucleotide polymorphisms of IL-4 C589T contribute to risk for asthma

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References

    1. Makoui MH, Imani D, Motallebnezhad M, Azimi M, Razi B. Vitamin D receptor gene polymorphism and susceptibility to asthma: meta-analysis based on 17 case-control studies. Ann Allergy Asthma Immunol. 2020;124(1):57–69. doi: 10.1016/j.anai.2019.10.014. - DOI - PubMed
    1. Peters SP, Ferguson G, Deniz Y, Reisner C. Uncontrolled asthma: a review of the prevalence, disease burden and options for treatment. Respir Med. 2006;100(7):1139–1151. doi: 10.1016/j.rmed.2006.03.031. - DOI - PubMed
    1. Subbarao P, Mandhane PJ, Sears MR. Asthma: epidemiology, etiology and risk factors. Cmaj. 2009;181(9):E181–E190. doi: 10.1503/cmaj.080612. - DOI - PMC - PubMed
    1. Sykes A, Johnston SL. Etiology of asthma exacerbations. J Allergy Clin Immunol. 2008;122(4):685–688. doi: 10.1016/j.jaci.2008.08.017. - DOI - PubMed
    1. Ober C, Yao TC. The genetics of asthma and allergic disease: a 21st century perspective. Immunol Rev. 2011;242(1):10–30. doi: 10.1111/j.1600-065X.2011.01029.x. - DOI - PMC - PubMed

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