Research Article: Association of the IL-1RN variable number of tandem repeat polymorphism and Helicobacter pylori infection: A meta-analysis

Date Published: April 6, 2017

Publisher: Public Library of Science

Author(s): Jinhua Zhang, Xudong Sun, Jiemin Wang, Fuhua Zhang, Xiaohua Li, Jian Han, Qingyi Wei.

http://doi.org/10.1371/journal.pone.0175052

Abstract

The aim of this study was to clarify the association of IL-1RN variable number of tandem repeat (VNTR) polymorphism and H. pylori infection. We performed a meta-analysis of studies retrieved by systematic searches of Pubmed, Embase and the Cochrane Library. Data were analyzed with STATA 13.1 using pooled odds ratios (ORs) with 95% confidence intervals (CIs). A total of 18 studies were included in our meta-analysis, and IL-1RN VNTR was found to be significantly associated with H. pylori infection in the comparisons of 22+2L vs. LL (OR = 1.17, 95% CI = 1.02–1.33) and 2 allele vs. L allele (OR = 1.18, 95% CI = 1.00–1.40). Stratified analyses on study designs and ethnicities were also conducted. IL-1RN VNTR was positively correlated with H. pylori infection in Asian subgroup and Hospital-Based subgroup (i.e., study samples obtained from hospital inpatients). In conclusion, our study demonstrated that IL-1RN VNTR polymorphism might increase the risk of H. pylori infection, especially in Asians.

Partial Text

Helicobacter pylori is a pathogen that was discovered by Warren and Marshall in 1983 [1], and is thought to be involved in gastritis, peptic ulcers, gastric cancer, and mucosa-associated lymphoid tissue (MALT) lymphoma [2–4]. More than half of the world’s population is infected with H. pylori. Multiple factors influence the outcomes of H. pylori infection. Host genetic factors, interacting with H. pylori virulence (VacA, CagA etc.), and environmental factors (high salt intake and nitrate consumption, etc.), are involved in the pathogenesis of gastric cancer [5–7]. H. pylori infection elicits adaptive and innate immune responses in the gastric mucosa that produce significant inflammation [6]. H. pylori can stimulates host secretion of cytokines including interleukin (IL)-1, -2, -4, -8, -10, -1 receptor antagonist (rα), tumor necrosis factor (TNF)-α and others that may contribute to persistent infection [6, 8–10]. Host genetic polymorphisms of several cytokine genes (e.g., IL-1B-511*T, IL-1-RN*2, IL-10-1082/-819/-592, TNF-A-308*A, and IL-8-251*A), innate immune response gene (TLR4+896*G), HLA (DQA1*03:01, DQA1*04:01, and DQB1*05:01:01) are involved in all stages of the neoplastic process in gastric carcinoma [6, 11–16]. Previous reports of the relationship of host genetic polymorphisms and H. pylori susceptibility are inconsistent. To begin to address these inconsistencies, we previously conducted two meta-analysis of the relationship between host IL1B -31C > T and TNFA gene polymorphisms and H. pylori infection [9, 10]. This meta-analysis focuses on the association of host IL-1RN variable number of tandem repeat (VNTR) polymorphism and H. pylori infection.

Previous studies demonstrated that polymorphisms of some host cytokine genes such as IL-1β, IL-8 et al. are correlated with H. pylori infection related-diseases [17, 44, 45]. IL-1rα can influence IL-1β levels, and some studies have focused on the relationship between IL-1RN VNTR polymorphism and H. pylori infection related-diseases [46, 47]. Others have investigated the association between IL-1RN VNTR polymorphism and H. pylori infection. Because the conclusions of the available studies were not consistent [9, 48], we performed this meta-analysis to investigate the role of IL-1RN VNTR polymorphism on the risk for H. pylori infection.

Based on including studies of our meta-analysis, we concluded that IL-1RN VNTR*2 may increase the risk of H. pylori infection, especially in Asians. Our findings provide insights into the role of IL-1RN VNTR polymorphism in H. pylori infection and related diseases. Further studies with larger sample sizes and various ethnicities are required to validate these results.

 

Source:

http://doi.org/10.1371/journal.pone.0175052

 

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