Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2017 Jun 9;7(1):3199.
doi: 10.1038/s41598-017-03523-0.

Association of Interleukin-12A rs568408 with Susceptibility to Asthma in Taiwan

Te-Chun Shen  1   2   3 , Chia-Wen Tsai  2 , Wen-Shin Chang  2 , Shengyu Wang  4 , Che-Yi Chao  5 , Chieh-Lun Hsiao  2 , Wei-Chun Chen  2   3   6 , Te-Chun Hsia  7   8   9 , Da-Tian Bau  10   11   12
Affiliations

Association of Interleukin-12A rs568408 with Susceptibility to Asthma in Taiwan

Te-Chun Shen et al. Sci Rep. .

Abstract

Asthma is an inflammatory disease and interleukin 12 (IL-12) may play a regulatory role in allergen-induced inflammation. The aim of this study was to investigate the association of polymorphisms in IL-12A/IL-12B with asthma. The asthma group included 198 adult patients and the control group included 453 individuals without asthma that were frequency-matched by gender and age. The distribution of genotypic and allelic frequencies of IL-12A rs568408 demonstrated significant differences between case and control groups. Specifically, the percentages of AA genotype of IL-12A rs568408 was significantly higher among asthmatic patients in Taiwan than healthy controls, compared to GG genotype. No significant difference was observed among the IL-12A rs2243115 and IL-12B rs3212227 genotypes between case and control groups. In addition, the A allele at IL-12A rs568408 was associated with more severe symptoms (P = 0.0085) among asthmatic patients. These results suggest that IL-12A rs568408 may contribute to the etiology and symptoms severity of asthma, indicating its usefulness as a predictive and diagnostic biomarker of asthma.

PubMed Disclaimer

Conflict of interest statement

The authors declare that they have no competing interests.

References

    1. Holgate ST. Genetics and environmental interactions in allergy and asthma. J Allergy Clin Immunol. 1999;104:1139–46. doi: 10.1016/S0091-6749(99)70005-9. - DOI - PMC - PubMed
    1. Lai T, et al. Interleukin-31 expression and relation to disease severity in human asthma. Sci Rep. 2016;6:22835. doi: 10.1038/srep22835. - DOI - PMC - PubMed
    1. Wardlaw AJ, et al. New insights into the relationship between airway inflammation and asthma. Clin Sci. 2002;103:201–11. doi: 10.1042/cs1030201. - DOI - PubMed
    1. Steinke JW, Rich SS, Borish L. Genetics of allergic disease. J Allergy Clin Immunol. 2008;121:S384–7. doi: 10.1016/j.jaci.2007.07.029. - DOI - PubMed
    1. Himes BE, et al. Genome-wide association analysis identifies PDE4D as an asthma susceptibility gene. Am J Hum Genet. 2009;84:581–93. doi: 10.1016/j.ajhg.2009.04.006. - DOI - PMC - PubMed

Publication types

Substances