Analysis of IL-33 Gene Polymorphisms (rs1157505C/G and rs11792633C/T) and the Risk of Tuberculosis in Southeastern Iran

Document Type : Research Article

Authors

1 Department of Biology, University of Sistan and Baluchestan, Zahedan, Iran

2 South Iranian Genetic Medical Center, Shiraz University of Medical Sciences, Shiraz, Iran

Abstract

Tuberculosis is a vagarious infectious disease that generally affects the lungs. Accordingly, in some cases, it can also affect the liver and kidney. Host genetic may affect tuberculosis caused by bacillus Mycobacterium tuberculosis. The main risk factors for the disease are a weakened immune system because of diabetes, some cancers, HIV/AIDS, severe kidney disease, cancer treatment, and malnutrition. Il-33 is involved in the activation of eosinophils, mast cells, basophils, and natural killer cells and the maturation of T helper type2 cells. The developments of CD4 (+) TH1 and CD8 (+) T cell responses are involved in protection against TB, IL-33 promotes the development of these cells. The purpose of the present research was to investigate the association between Mycobacterium tuberculosis infection and IL-33 gene polymorphisms (rs1157505C/G and rs11792633C/T) with tuberculosis in the cases and controls from the area of high tuberculosis prevalence in Iran. In this study, 100 patients with tuberculosis disease and 91 healthy controls were included. Polymorphisms of the IL-33 gene were genotyped using T-ARMS-PCR. The analysis of the haplotype combinations among IL-33 polymorphisms demonstrated that the magnitude of the association was higher for the combined CC/CT genotypes. The CT genotype related to C/T polymorphism of the IL-33 gene increased the risk of tuberculosis. The combined CG+GG genotypes related to C/G polymorphism of the IL-33 gene also increased the risk of tuberculosis, but the difference was not statistically significant. In conclusion, IL-33 gene polymorphisms may be considered as important contributors to tuberculosis in Iran.

Keywords

References

Azazi EA, Elshora AE, Tantawy EA, Elsayd MA. 2014. Serum levels of Interleukin-33 and its soluble receptor ST2 in asthmatic patients. Egypt J Chest Dis Tuberc 63(2): 279-284.
Blok DC, Kager LM, Hoogendijk AJ, Lede IO, Rahman W, Afroz R, de Jong MD. 2015. Expression of inhibitory regulators of innate immunity in patients with active tuberculosis. BMC Infect Dis 15(1): 98. doi: 10.1186/s12879-015-0833-z.
Carriere V, Roussel L, Ortega N, Lacorre DA, Americh L, Aguilar L, Girard JP. 2007. IL-33, the IL-1-like cytokine ligand for ST2 receptor, is a chromatin-associated nuclear factor in vivo. Proc Natl Acad Sci 104: 282-287.
Cayrol C, Girard JP. 2014. IL-33: an alarmin cytokine with crucial roles in innate immunity, inflammation and allergy. Curr Opin Immunol 31: 31-37.
Flynn JL, Chan J. 2001. Tuberculosis: latency and reactivation. Infect Immun 69: 4195-4201.
Getahun H, Gunneberg C, Granich R, Nunn P. 2010. HIV infection-associated tuberculosis: the epidemiology and the response. Clin Infect Dis 50 Suppl 3: S201-207.
Gudbjartsson DF, Bjornsdottir US, Halapi E, Helgadottir A, Sulem P, Jonsdottir GM, Williams C. 2009. Sequence variants affecting eosinophil numbers associate with asthma and myocardial infarction. Nat Genet 41: 342-347.
Kurowska‐Stolarska M, Hueber A, Stolarski B, McInnes IB. 2011. Interleukin‐33: a novel mediator with a role in distinct disease pathologies. J Intern Med 269: 29-35
Lee KS, Kim HR, Kwak S, Choi KH, Cho JH, Lee YJ, Park DS. 2013. Association between elevated pleural interleukin-33 levels and tuberculous pleurisy. Ann Lab Med 33: 45-51.
Miller AM. 2011. Role of IL-33 in inflammation and disease. doi: 10.1186/1476-9255-8-22
Moosazadeh M, Khanjani N, Bahrampour A, Nasehi M. 2014. Does tuberculosis have a seasonal pattern among migrant population entering Iran? Int J Health Policy Manag 2: 181-185.
Moussion C, Ortega N, Girard JP. 2008. The IL-1-like cytokine IL-33 is constitutively expressed in the nucleus of endothelial cells and epithelial cells in vivo: a novel ‘alarmin’? PLoS One 3: e3331.
Oshikawa K, Kuroiwa K, Tago K, Iwahana H, Yanagisawa KEN, Ohno S, Sugiyama Y. 2001. Elevated soluble ST2 protein levels in sera of patients with asthma with an acute exacerbation. Am J Respir Crit Care Med 164: 277-281.
Raja A. 2004. Immunology of tuberculosis. Indian J Med Res 120: 213-232.
Sakashita M, Yoshimoto T, Hirota T, Harada M, Okubo K, Osawa Y, Tamari M. 2008. Association of serum interleukin‐33 level and the interleukin‐33 genetic variant with Japanese cedar pollinosis. Clin Exp Allergy 38: 1875-1881.
Schluger NW, Rom WN. 1998. The host immune response to tuberculosis. Am J Respir Crit Care Med. 157(3): 679-691
Schmitz J, Owyang A, Oldham E, Song Y, Murphy E, McClanahan TK, Gorman DM. 2005. IL-33, an interleukin-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines. Immunity 23: 479-490.
Smith DE. 2010. IL-33: a tissue derived cytokine pathway involved in allergic inflammation and asthma. Clin Exp Allergy 40: 200-208.
Tajima S, Oshikawa K, Tominaga SI, Sugiyama Y. 2003. The increase in serum soluble ST2 protein upon acute exacerbation of idiopathic pulmonary fibrosis. Chest 124: 1206-1214.
Yagami A, Orihara K, Morita H, Futamura K, Hashimoto N, Matsumoto K, Matsuda A. 2010. IL-33 mediates inflammatory responses in human lung tissue cells. J Immunol 185: 5743-5750.
Zumla A, George A, Sharma V, Herbert N. 2013. WHO's 2013 global report on tuberculosis: successes, threats, and opportunities. Lancet 382: 1765-1767.
Zumla A, Rao M, Parida SK, Keshavjee S, Cassell G, Wallis R, Maeurer M. 2015. Inflammation and tuberculosis: host‐directed therapies. J Intern Med 277: 373-387.
Journal of Genetic Resources
Volume 6, Issue 1
February 2020
Pages 54-59

Files

Share

How to cite

Statistics