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Review paper

Interleukin-8 heterozygous polymorphism (-251 T/A and +781 C/T) increases the risk of Helicobacter pylori-infection gastritis in children: a case control study

By
Dr Supriatmo Orcid logo ,
Dr Supriatmo
Contact Dr Supriatmo

Department of Child Health, School of Medicine, Universitas Sumatera Utara , Medan , Indonesia

Gontar Alamsyah Siregar ,
Gontar Alamsyah Siregar

Department of Internal Medicine, School of Medicine, Universitas Sumatera Utara , Medan , Indonesia

Iqbal Pahlevi Adeputra Nasution ,
Iqbal Pahlevi Adeputra Nasution

Department of Surgery, School of Medicine, Universitas Sumatera Utara , Medan , Indonesia

Oke Rina Ramayani
Oke Rina Ramayani

Department of Child Health, School of Medicine, Universitas Sumatera Utara , Medan , Indonesia

Abstract

Aim
To investigate the effects of interleukin-8 (IL-8)-251 T/A and +781 C/T polymorphism on the risk of Helicobacter pyloriinfection gastritis in children, and the IL-8 level of children with or without gastritis H. pylori infection according to polymorphism.
Methods
This prospective, case control clinical study included 64 children 2-18 years old. A disease group (32 gastritis patients with H. pylori-infection) was compared with a control group (32 gastritis patients without H. pylori infection). Demographic characteristics of patients were taken by a questionnaire; gastritis was confirmed by gastroscopy, H. pylori infection was confirmed with rapid urease test. Serum IL-8 level was measured by ELISA, and IL-8-251 T/A and +781 C/T polymorphisms were analysed by RT-PCR. Demographic characteristics, IL-8 level, polymorphism of patients, and IL-8 level according to polymorphisms were compared between the groups.
Results
Children with tobacco exposure were associated with an increased risk of H. pylori-infection gastritis by 3.4-fold. There was a higher IL-8 level in the disease group compared to the control group. The disease group with IL-8-251 AT polymorphism had a higher risk compared to TT polymorphism by 8.7-fold, and with IL-8 +781 CT polymorphism had a higher risk compared to CC polymorphism by 10.7-fold. Children in the disease group with IL-8-251 AT and TT, and +781 CT and CC polymorphisms produced a higher IL-8 level than the control group in respective polymorphisms.
Conclusion
Children with H. pylori-infection gastritis have higher IL-8 production. There was an increased risk of developing H. pylori-infection in heterozygous-251 AT and +781 CT.

References

1.
Torbenson M. Surgical Pathology of Non-neoplastic Gastrointestinal Diseases. 2019;121–35.
2.
Park Y, Kim N. Review of atrophic gastritis and intestinal metaplasia as a premalignant lesion of gastric cancer. J Cancer Prev. 2015;25–40.
3.
Azer S, Akhondi H, Gastritis. StatPearls Treasure Island (FL): StatPearls Publishing; 2020. 28AD;
4.
Kao CY, Sheu BS, Wu JJ. Helicobacter pylori infection: an overview of bacterial virulence factors and pathogenesis. Biomed J. 2016;14–23.
5.
Saes M, De Labio R, Rasmussen L, Payão S. Interleukin 8 (-251 T>A) polymorphism in children and teenagers infected with Helicobacter pylori. J Venom Anim Toxins Incl Trop Dis. 2017;23.
6.
Kamali-Sarvestani E, Bazargani A, Masoudian M, Lankarani K, Taghavi AR, Saberifiroozi M. Association of H pylori cagA and vacA genotypes and IL-8 gene polymorphisms with clinical outcome of infection in Iranian patients with gastrointestinal diseases. World J Gastroenterol. 2006;5205–10.
7.
Hull J, Ackerman H, Isles K, Usen S, Pinder M, Thomson A, et al. Unusual haplotypic structure of IL8, a susceptibility locus for a common respiratory virus. Am J Hum Genet. 2001;413–9.
8.
Ohyauchi M, Imatani A, Yonechi M, Asano N, Miura A, Iijima K, et al. The polymorphism interleukin 8 -251 A/T influences the susceptibility of Helicobacter pylori related gastric diseases in the Japanese population. Gut. 2005;330–5.
9.
Chang Y, Oh C, Kim JW, Lee J, Park M, Shim JJ, et al. Combination of Helicobacter pylori infection and the interleukin 8 -251 T > A polymorphism, but not the mannose-binding lectin 2 codon 54 G > A polymorphism, might be a risk factor of gastric cancer. BMC Cancer. 2017;388.
10.
Ramis I, Vianna J, Gonçalves C, Groll V, Dellagostin A, Da Silva O, et al. Polymorphisms of the IL-6, IL-8 and IL-10 genes and the risk of gastric pathology in patients infected with Helicobacter pylori. J Microbiol Immunol Infect. 2017;153–9.
11.
Abbas I. Interleukin-8 251-A/T polymorphism related to peptic ulcer disease in H. pylori infected patient. Journal of Contemporary Medical Sciences. 2016;138–40.
12.
Rafrafi A, Chahed B, Kaabachi S, Kaabachi W, Maalmi H, Hamzaoui K, et al. Association of IL-8 gene polymorphisms with non small cell lung cancer in Tunisia: a case control study. Hum Immunol. 2013;1368–74.
13.
Zarafshani MK, Shahmohammadi A, Vaisi-Raygani A, Bashiri H, Yari K. Association of interleukin-8 polymorphism (+781 C/T) with the risk of ovarian cancer. Meta Gene. 2018;165–9.
14.
Savage S, Abnet C, Mark S, Qiao YL, Dong ZW, Dawsey S, et al. Variants of the IL8 and IL8RB Genes and risk for gastric cardia adenocarcinoma and esophageal squamous cell carcinoma. Cancer Epidemiol Biomarkers Prev. 2004;2251–7.
15.
Sugimoto M, Yamaoka Y, Furuta T. Influence of interleukin polymorphisms on development of gastric cancer and peptic ulcer. World J Gastroenterol. 2010;1188–200.
16.
Fu J, Wang K, Qi S. Role of IL-8 gene polymorphisms in glioma development in a Chinese population. Genet Mol Res. 2016;
17.
Liu H, Mao P, Xie C, Xie W, Wang M, Jiang H. Association between interleukin 8-251 T/A and +781 C/T polymorphisms and glioma risk. Diagn Pathol. 2015;138–138.
18.
Chen Y, Yang Y, Liu S, Zhu S, Jiang H, Ding J. Association between interleukin 8 -251 A/T and +781 C/T polymorphisms and osteosarcoma risk in Chinese population: a case-control study. Tumor Biol. 2016;6191–6.
19.
Dibley M, Staehling N, Nieburg P, Trowbridge F. Interpretation of Z-score anthropometric indicators derived from the international growth reference. Am J Clin Nutr. 1987;749–62.
20.
Malaty H, Graham D. Importance of childhood socioeconomic status on the current prevalence of Helicobacter pylori infection. Gut. 1994;742–5.
21.
Kim Y, Kim H, Kim J, Lee D, Jung J, Cho S, et al. Association between environmental tobacco smoke and Helicobacter pylori infection in children and adolescents: the United States national health and nutritional examination survey 1999-2000. Korean J Fam Med. 2018;565–9.
22.
Korwin JD, De, Ianiro G, Gibiino G, Gasbarrini A. Helicobacter pylori infection and extragastric diseases in 2017. Helicobacter. 2017;12411.
23.
Du Y, Zhu H, Liu J, Li J, Chang X, Zhou L, et al. Consensus on eradication of Helicobacter pylori and prevention and control of gastric cancer in China. J Gastroenterol Hepatol. 2019;
24.
Dakal T, Kala D, Dhiman G, Yadav V, Krokhotin A, Dokholyan N. Predicting the functional consequences of non-synonymous single nucleotide polymorphisms in IL8 gene. Sci Rep. 2017;1–18.
25.
Ferreira R, Pinto-Ribeiro I, Wen X, Pinto M, Dinis-Ribeiro R, Carneiro M, et al. Helicobacter pylori cagA promoter region sequences influence CagA expression and interleukin 8 secretion. J Infect Dis. 2016;669–73.
26.
Lee H, Su YL, Huang BS, Hsieh FT, Chang YH, Tzeng SR, et al. Importance of the C-terminal histidine residues of Helicobacter pylori GroES for Tolllike receptor 4 binding and interleukin-8 cytokine production. Sci Rep. 2016;37367.
27.
Taguchi A, Ohmiya N, Shirai K, Mabuchi N, Itoh A, Hirooka Y, et al. Interleukin-8 promoter polymorphism increases the risk of atrophic gastritis and gastric cancer in Japan. Cancer Epidemiol Biomarkers Prev. 2005;2487–93.
28.
Kamangar F, Abnet C, Hutchinson A, Newschaffer C, Helzlsouer K, Shugart Y, et al. Polymorphisms in inflammation-related genes and risk of gastric cancer (Finland). Cancer Causes Control. 2006;117–25.

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