American Journal of Infectious Diseases and Microbiology
ISSN (Print): 2328-4056 ISSN (Online): 2328-4064 Website: Editor-in-chief: Maysaa El Sayed Zaki
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American Journal of Infectious Diseases and Microbiology. 2016, 4(5), 102-106
DOI: 10.12691/ajidm-4-5-2
Open AccessArticle

The Interleukin-8 -251 A Allele is Associated with Increased Risk of Different Gastroduodenal Diseases in H. pylori Infected Bangladeshi Patients

Ritu Saha1, , Md. Ashraful Islam2, Abu Naser Ibne Sattar1 and Sharmeen Ahmed1

1Department of Microbiology and Immunology, Bangabandhu Sheikh Mujib Medical University, Dhaka, Bangladesh

2Department of Gastroenterology, Dhaka Medical College Hospital, Dhaka, Bangladesh

Pub. Date: October 27, 2016

Cite this paper:
Ritu Saha, Md. Ashraful Islam, Abu Naser Ibne Sattar and Sharmeen Ahmed. The Interleukin-8 -251 A Allele is Associated with Increased Risk of Different Gastroduodenal Diseases in H. pylori Infected Bangladeshi Patients. American Journal of Infectious Diseases and Microbiology. 2016; 4(5):102-106. doi: 10.12691/ajidm-4-5-2


Persistent Helicobacter pylori infection leads to chronic inflammation of the gastric mucosa which is mediated by various inflammatory cytokines. Host susceptibility along with bacterial virulence factors are also regarded as contributing factor of developing severe H. pylori induced gastroduodenal diseases like peptic ulcer diseases and gastric adenocarcinoma. Polymorphisms in genes that code cytokines influence cytokine secretion levels. Of the inflammatory cytokines, Interleukin-8 (IL-8) plays an important role in gastric mucosal inflammation induced by H. pylori infection. The IL8 gene has been described as having a polymorphism of an A/T base pair in the promoting region (−251) which is associated with an increased synthesis of interleukin by gastric epithelial cells. So the study was conducted to investigate the association of IL-8–251 A/T polymorphism with gastroduodenal diseases in H. pylori infected Bangladeshi patients. Methods: Endoscopic gastroduodenal biopsy sample of 113 dyspeptic patients were used (54 was infected with H. pylori and 59 was not infected with H. pylori). H. pylori infection was detected by Rapid urease test, PCR of ureC gene and histology. Gastroduodenal disease was diagnosed by histopathological examination. Il-8 gene polymorphism (at -251 position) was detected by Polymerase Chain Reaction restriction fragment length polymorphism. Result: A significant association was found between host IL-8 genotypes (T/T, T/A, A/A and A carrier) and the presence of H. pylori infection (p =0.001). The IL-8 A allele carriers infected with H. pylori had an increased risk of developing gastritis (p =0.003) and peptic ulcer diseases (p= .002). We did not find a correlation between IL-8 gene polymorphism and a higher risk of gastric carcinoma and or precancerous lesions. Conclusion: The H. pylori infected patients carrying A allele may increase risk of developing gastritis and peptic ulcer disease in Bangladeshi patients.

Helicobacter pylori infection gastroduodenal disease Interleukin-8 Genetic polymorphism

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[1]  Montecucco C and Rappuoli R., “Living dangerously: how Helicobacter pylori survives in the human stomach”, Nature Reviews Molecular Cell. Biology, 2, 457-466, 2001.
[2]  Kang DW, Hwang WC, Park MH, Ko GH, Ha WS, Kim KS et al., “Rebamipide abolishes Helicobacter pylori CagA-induced phospholipase D1 expression via inhibition of NFκB and suppresses invasion of gastric cancer cells”, Oncogene, 32, 3531-3542, 2013.
[3]  Hwang IR, Kodama T, Kikuchi S, Sakai K, Peterson LE, Graham DY et al, “Effect of Interleukin 1 Polymorphisms on Gastric Mucosal Interleukin 1beta Production in Helicobacter pylori Infection”, Gastroenterology, 123 (6), 1793-1803, 2002.
[4]  Hatz RA, Brooks WP, Kra mling HJ, and Enders G, “Stomach immunology and Helicobacter pylori infection”, Current Opinion in Gastroenterology, 8, 993-1001, 1992.
[5]  Rieder G, Hatz RA, Moran AP, Walz A, Stolte M, “Role of Adherence in Interleukin-8 Induction in Helicobacter pylori -Associated Gastritis”, Infection and Immunity, 65(9), 3622-3630, 1997.
[6]  Yamaoka Y, Kita M, Kodama T, Sawai N, Tanahashi T, Kashima K et al., “Chemokines in the gastric mucosa in Helicobacter pylori infection”, Gut, 42, 609-617, 1998.
[7]  Yamaoka Y, Kodama T, Kita M, Imanishi J, Kashima K, Graham DY, “Relation between clinical presentation, Helicobacter pylori density, interleukin 1beta and 8 production, and cagA status”, Gut, 45, 804-811, 1999.
[8]  Crabtree JE, Lindley IJ, “Mucosal interleukin-8 and Helicobacter pylori-associated gastroduodenal disease”, European Journal of Gastroenterology & Hepatology, 6(suppl 1), S33-S38, 1994.
[9]  Taguchi A, Ohmiya N, Shirai K, Mabuchi N, Itoh A, Hirooka Y, Niwa Y, Goto H, “Interleukin-8 promoter polymorphism increases the risk of atrophic gastritis and gastric cancer in Japan”, Cancer Epidemiol Biomarkers Prev, 14, 2487-2493, 2005.
[10]  Vinagre RMDF, Corvelo TCO, Arnaud VC, Leite ACK, Barile KAS, Martins LC, “Determination of strains of Helicobacter pylori and of polymorphism in the interleukin-8 gene in patients with stomach cancer”, Arq Gastroenterol, 48(1),46-51, 2011.
[11]  Caleman Neto A, Rasmussen LT, de Labio RW, deQueiroz VF, Smith M de A, Viani GA et al, “Gene Polymorphism of Interleukin 1 and 8 in Chronic Gastritis Patients Infected with Helicobacter pylori, Journal of Venomous Animals and Toxins Including Tropical Diseases, 20 (17), 1-5, 2014.
[12]  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 , 54 (3), 330-335, 2005.
[13]  Ramis IB, Vianna JS, Gonçalves CV, Groll AV, Dellagostin OA, da Silva PE, “Polymorphisms of the IL-6, IL-8 and IL-10 Genes and the Risk of Gastric Pathology in Patients Infected with Helicobacter pylori, Journal of Microbiology, Immunology and Infection, Mar 24, 1-7, 2015.
[14]  Zhang L, Du C, Guo X, Yuan L, Niu W, Yu W et al., “Interleukin-8-251 A/T Polymorphism and Helicobacter pylori Infection Influence Risk for the Development of Gastric Cardiac Adenocarcinoma in a High-Incidence Area of China”, Molecular Biology Reports, 37 (8), 3983-3989, 2010.
[15]  Savage SA, Hou L, Lissowska J, Chow WH, Zatonski W, Chanock SJ et al, “Interleukin-8 polymorphisms are not associated with gastric cancer risk in a Polish population”, Cancer Epidemiology ang Biomarkers Preview, 15, 589-591, 2006.
[16]  Kamangar F, Abnet CC, Hutchinson AA, et al., “Polymorphisms in inflammation-related genes and risk of gastric cancer (Finland)”, Cancer Causes Control,17, 117-125, 2006.
[17]  Ye BD, Kim SG, Park JH, Kim JS, Jung HC, Song IS, “The interleukin-8-251 A allele is associated with increased risk of noncardia gastric adenocarcinoma in Helicobacter pylori infected Koreans”, J Clin Gastroenterol, 43, 233e9, 2009.
[18]  Tongtawee T, Kaewpitoon S, Kaewpitoon N, Dechsukhum C, Loyd RA, Matrakool L, “Correlation between Gastric Mucosal Morphologic Patterns and Histopathological Severity of Helicobacter pylori Associated Gastritis Using Conventional Narrow Band Imaging Gastroscopy”, Biomedical Research International, 2015, 1-7, 2015.
[19]  Akada JK., Ogura K, Dailidiene D, Dailide G, Cheverud JM, Berg DE, “Helicobacter pylori tissue tropism: mouse-colonizing strains can target different gastric niches”, Microbiology, 149: 1901-1909, 2003.
[20]  Salih BA, Bolek BK, Arikan S, “DNA sequence analysis of cagA 3 ‘ motifs of Helicobacter pylori strains from patients with peptic ulcer diseases”, J Med Microbiol, 59(2), 144-148, 2010.
[21]  Lu JJ, Perng CL, Shyu RY, Chen CH, Lou Q, Chong KF et al, “Comparison of Five PCR Methods for Detection of Helicobacter pylori DNA in Gastric Tissues”, Journal of Clinical Microbiology, 37 (3), 772-774, 1999.
[22]  Rad R, Dossumbekova A, Neu B, Lang R, Bauer S, Saur D et al., “Cytokine gene polymorphisms influence mucosal cytokine expression, gastric inflammation, and host specific colonisation during Helicobacter pylori infection”, Gut, 53(8), 1082-1089, 2004.
[23]  Fabris RD, Rasmussen LT, Caleman Neto A, Lábio RW, Orcini W, Ximenez JP et al, “Polimorfismo da Interleucina-8-251T> A e Helicobacter pylori, ACM arq. catarin. med, 40(3), 25-29, 2011.
[24]  Farshad S, Rasouli M, Jamshidzadeh A, Hosseinkhani A, Japoni A, Alborzi A et al., “IL-1ß (+3953 C/T) and IL-8 (-251 A/T) Gene Polymorphisms in H. pylori Mediated Gastric Disorders”, Iranian Journal of Immunology, IJI 7 (2), 96-108, 2010.
[25]  Xue H, Liu J, Lin B, Wang Z, Sun J, and Huang G, “A Meta-Analysis of Interleukin-8 -251 Promoter Polymorphism Associated with Gastric Cancer Risk”, PLoS ONE, 7 (1), 2012.
[26]  Thye T, Burchard GD, Nilius M, Müller-Myhsok B, Horstmann RD, “Genomewide linkage analysis identifies polymorphism in the human interferon-γ receptor affecting Helicobacter pylori infection”, The American Journal of Human Genetics, 72(2), 448-453, 2003.
[27]  Hofner P, Gyulai Z, Kiss ZF, Tiszai A, Tiszlavicz L, Tóth G, Szõke D, Molnár B, Lonovics J, Tulassay Z, Mándi Y, “Genetic Polymorphisms of NOD1 and IL‐8, but not Polymorphisms of TLR4 Genes, Are Associated with Helicobacter pylori‐Induced Duodenal Ulcer and Gastritis” Helicobacter, 12(2),124-31, 2007.
[28]  Gyulai Z, Klausz G, Tiszai A, Lénárt Z, Kása IT, Lonovics J, Mándi Y, “Genetic polymorphism of interleukin-8 (IL-8) is associated with Helicobacter pylori-induced duodenal ulcer. European cytokine network”., 15(4), 353-8, 2004.
[29]  Kamali-Sarvestani E, Bazargani A, Masoudian, 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 Journal of Gastroenterology, 12 (32), 5205-5210, 2006.
[30]  Sugimoto M, Yamaoka Y, and Furutan T, “Influence of Interleukin Polymorphisms on Development of Gastric Cancer and Peptic Ulcer”, World Journal of Gastroenterology, 16 (10), 1188-1200, 2010.
[31]  Costa A, Figueiredo C, Touati E, “Pathogenesis of Helicobacter pylori Infection”, Helicobacter, 14, 15-20, 2009.
[32]  McLean M & El-Omar E, “Genetic aspects of inflammation”, Current Opinion In Pharmacology, 9(4), 370-374, 2009.