Volume 11, Issue 2 (Vol.11 No.2 Jul 2022)                   rbmb.net 2022, 11(2): 344-349 | Back to browse issues page


XML Print


Department of Biology, College of science, Babylon University, Iraq.
Abstract:   (1857 Views)
Background: Bronchial asthma has a complicated genetic history. Changes in gene expression may be caused by gene polymorphism, cytokines play a central role. IL-13 is an interleukin that has been shown to play a role in the disease's immunopathogenesis. The current study investigated the relationship between rs20541 of the IL-13 gene and Bronchial asthma in Iraqi patients.

Methods: Seventy-five patient and fifty healthy individuals as a control. The DNA was extracted from blood samples. Detection of genotype IL-13SNP (rs20541) were achieved by RFLP-PCR. 

Results: indicated a highly significant the levels of the IgE, and IL-13 in the patients compared to control at (p value≤ 0.01), (456.45±290.106 vs. 30.08±24.414), (59.5980±20.93750 vs.6.7034±4.10547) pg/ml respectively. Result shows no significant differences in the frequency distributions of IL-13 SNP (rs20541) for all genotypes in cases and controls. A protective role of asthma, (OR: 0.62; CI.95%: 0.23 - 1.6) and (OR 0.89; CI.95%:0.42 - 1.89) were observed for wild type homozygous and heterozygous genotype respectively. Whereas the AA genotype (42.7%) in cases and (34.0%) in control, that (OR:1.44; CI.95%:( 0.66 - 3.07) mutant homozygous were risk factors of asthma among individuals. The genotypes of IL-13 rs20541 (GG, AG, AA) among patients and controls were significantly correlated with IgE and IL-13 results at (p≤ 0.05). 

Conclusions: AA genotype in case and control mutant homozygous were risk factors of asthma among individuals. It’s possible that this has a predisposing impact on the development of asthma.
Full-Text [PDF 358 kb]   (1286 Downloads)    
Type of Article: Original Article | Subject: Molecular Biology
Received: 2022/03/26 | Accepted: 2022/03/29 | Published: 2022/08/7

References
1. McGregor MC, Krings JG, Nair P, Castro M. Role of biologics in asthma. American Journal of Respiratory and Critical Care Medicine. 2018;199(4):433-445. [DOI:10.1164/rccm.201810-1944CI] [PMID] [PMCID]
2. Reuter S, Stassen M, Taube C. (2010). Mast cells in allergic asthma and beyond. Yonsei Med J. 2010;51(6):797-807. [DOI:10.3349/ymj.2010.51.6.797] [PMID] [PMCID]
3. Gould H J, Sutton BJ, Beavil AJ, Beavil R, McCloskey N, Coker HA, Fear D, Smurthwaite L. The biology of IGE and the basis of allergic disease. Annu Rev Immunol. 2003;21:579-628.Halwani R, Vazquez-Tello A, Kenana R, Al-Otaibi M, Alhasan KA, Shakoor Z, Al- Muhsen S. Association of IL-13 rs20541 and rs1295686 variants with symptomatic asthma in a Saudi Arabian population. J Asthma. 2018;55(11):1157-1165. [DOI:10.1080/02770903.2017.1400047] [PMID]
4. Gallagher G, Eskdale J, Bidwell J. Cytokine genetics-polymorphisms, functional variations and disease associations. The Cytokine Handbook. 2003. [DOI:10.1016/B978-012689663-3/50006-5]
5. DeMeo DL, Lange C, Silverman E, Senter K, J M, Drazen, J. M, Barth, M. J, Laird, N, & Weiss, S. T. (2002). Univariate and multivariate family‐based association analysis of the IL‐13 ARG130GLN polymorphism in the Childhood Asthma Management program. Genet Epidemiol. 2002;23(4):335-48. [DOI:10.1002/gepi.10182] [PMID]
6. Loza MJ, Chang B-L. Association between Q551R IL4R genetic variants and atopic asthma risk demonstrated by meta-analysis. J Allergy Clin Immunol. 2007;120(3):578-85. [DOI:10.1016/j.jaci.2007.05.019] [PMID]
7. Shazia M, Kanza M, Mehwish I, Irum S, Farida A, Asifa A. IL-13 gene polymorphisms and their association with atopic asthma and rhinitis in Pakistani patients. Iran J Allergy Asthma Immunol. 2013;12(4):391-6.
8. Sambrook, J. & Russell, D. W. (2001). Molecular cloning: a laboratory manual (Vol. 1). Cold Spring Harbor Laboratory Cold Spring Harbor, NY.
9. IBM Corp. Released 2017. IBM SPSS Statistics for Windows, Version 25.0. Armonk, NY: IBM Corp.
10. Mahmood, N. S, & Abdulla, A. A. (2021). Association of IL-4− 590 (C> T) Gene polymorphism with the Levels of Serum IL-4 and IgE on the Risk of Bronchial Asthma in Babylon Province/Iraq. Annals of the Romanian Society for Cell Biology, 391-400.
11. Medoff BD, Thomas SY, Luster AD. T cell trafficking in allergic asthma: the ins and outs. Annu Rev Immunol. 2008;26:205-32. [DOI:10.1146/annurev.immunol.26.021607.090312] [PMID]
12. Marone G. Asthma: recent advances. Immunol Today. 1998;19(1):5-9. [DOI:10.1016/S0167-5699(97)01187-0]
13. Elias JA, Zheng T, Lee CG, Homer RJ, Chen Q, Ma B, Blackburn M, Zhu Z. Transgenic modeling of interleukin-13 in the lung. Chest. 2003;123(3 Suppl):339S-45S. [DOI:10.1378/chest.123.3_suppl.339S] [PMID]
14. Gerald JK, Gerald LB, Vasquez MM, Morgan WJ, Boehmer SJ, Lemanske Jr RF, et al. Markers of differential response to inhaled corticosteroid treatment among children with mild persistent asthma. J Allergy Clin Immunol Pract. 2015;3(4):540-6.e3. [DOI:10.1016/j.jaip.2015.01.023] [PMID] [PMCID]
15. Froidure A, Mouthuy J, Durham S R, Chanez P, Sibille Y, Pilette C. Asthma phenotypes and IgE responses. European Respiratory Journal. 20106;47:304-319. [DOI:10.1183/13993003.01824-2014] [PMID]
16. Postma DS, Bleecker ER, Amelung PJ, Holroyd KJ, Jianfeng Xu, Panhuysen CIM, et al. Genetic susceptibility to asthma-bronchial hyperresponsiveness coinherited with a major gene for atopy. New England Journal of Medicine. 1995;333:894-900. [DOI:10.1056/NEJM199510053331402] [PMID]
17. Shirkani A, Mansouri A, Hosseini RF, Azad FJ, Mahmoudian R AL, Montazer MM, et al. The Role of Interleukin-4 and 13 Gene Polymorphisms in Allergic Rhinitis: A Case Control Study. Rep Biochem Mol Biol. 2019;8(2):111-118.
18. Howard TD, Whittaker PA, Zaiman AL, Koppelman G H, Xu J, Hanley M T, et al. Identification and association of polymorphisms in the interleukin-13 gene with asthma and atopy in a Dutch population. Am J Respir Cell Mol Biol. 2001;25(3):377-384. [DOI:10.1165/ajrcmb.25.3.4483] [PMID]

Rights and permissions
Creative Commons License This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.