Associations between cytokine gene polymorphisms and susceptibility to Helicobacter pylori infection and Helicobacter pylori related gastric cancer, peptic ulcer disease: A meta-analysis.

Jingjing Ma,Xue Hu,Mingwei Cao,Jiao Li,Dandan Wu,Weiguo Dong

doi:10.1371/journal.pone.0176463

Jingjing Ma, Xue Hu + Show 4 more

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Journal: PLOS ONE	Publication Date: Apr 28, 2017
Citations: 33	License type: CC BY 4.0

Affiliation: Wuhan University, Renmin Hospital of Wuhan University

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ObjectivesThe aim of this study is to clarify the associations between IL-1B31C/T, IL-1B-511C/T, IL-8-251T/A gene polymorphisms and the risk of Helicobacter pylori (H. pylori) infection together with H. pylori-related gastric cancer (GC), peptic ulcer disease (PUD).MethodsAll eligible literature published up to July 2016 were identified by searching Pubmed, Embase, Web of Science and CNKI. Pooled odds ratio (OR) and 95% confidence interval (95% CI) were calculated using a fixed or random effects model.Results29 case-control studies were eligible, and each of them may focus on more than one gene polymorphism. Ultimately, there were 21 studies (3159 cases and 2816 controls) for IL-1B-31C/T, 16 studies (2486 cases and 1989 controls) for IL-1B-511C/T polymorphisms, 9 studies (1963 cases and 1205 controls) for IL-8-251T/A polymorphisms. Overall, an increased risk of H. pylori infection was found for IL-1B-31C/T polymorphisms in total population [OR = 1.134, 95%CI = 1.008–1.275 for recessive model; OR = 1.145, 95%CI = 1.007–1.301 for TT vs CC model]. While, for IL-1B-511C/T and IL8-251T/A polymorphisms, no evidence indicated that they were associated with the risk of H. pylori infection in all genetic models. Furthermore, we found an increased risk of H. pylori-related GC with IL-1B-511C/T polymorphisms [OR = 1.784, 95%CI = 1.289–2.469 for recessive model; OR = 1.772, 95%CI = 1.210–2.594 for TT vs CC model] and IL8-251A/T polymorphisms [OR = 1.810, 95%CI = 1.229–2.667 for recessive model; OR = 1.717, 95%CI = 1.143–2.580 for TT vs AA model], an increased risk of H. pylori-related PUD with IL8-251T/A polymorphisms [OR = 1.364, 95%CI = 1.010–1.843 for recessive model; OR = 1.427, 95%CI = 1.039–1.959 for AA vs TT model].ConclusionsIL-1B-31C/T gene polymorphisms might increase H. pylori infection risk. IL-1B-511-C/T and IL-8-251T/A gene polymorphisms might act as a risk factor to H. pylori-related diseases including GC or PUD

Highlights

Helicobacter pylori (H. pylori) is well known as a special bacterium that usually establishes in the human stomach, which is a special etiological factor of various gastro-duodenal diseases, including chronic gastritis, peptic ulcer disease (PUD) including gastric ulcer and duodenal ulcer, some forms of gastric cancer(GC), even colonic cancer and pancreatic cancer[1,2,3,4]
An increased risk of H. pylori infection was found for IL-1B-31C/T polymorphisms in total population [odds ratio (OR) = 1.134, 95%CI = 1.008–1.275 for recessive model; OR = 1.145, 95%CI = 1.007–1.301 for TT vs CC model]
For IL-1B-511C/T and IL8-251T/A polymorphisms, no evidence indicated that they were associated with the risk of H. pylori infection in all genetic models

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Helicobacter pylori (H. pylori) is well known as a special bacterium that usually establishes in the human stomach, which is a special etiological factor of various gastro-duodenal diseases, including chronic gastritis, peptic ulcer disease (PUD) including gastric ulcer and duodenal ulcer, some forms of gastric cancer(GC), even colonic cancer and pancreatic cancer[1,2,3,4]. Increasing researches indicated that genetic factors that regulate cytokine production can effect an individual’s susceptibility to H. pylori infection, which plays a major role in the pathogenic process of H. pylori-related diseases such as PUD, GC [8,9]. IL-1β (encoded by IL-1B gene) is involved in many cellular activities including inflammatory response and secretion of gastric acid [12,13]. It has been shown IL-1B-31C/T and IL-1B511C/T polymorphisms are closely related to GC, they are found to more frequently occur in Chinese GC patients [14,15]. The -31C allele of IL-1B seems to be as a potent depressor of gastric acid secretion, IL-1β is a 100-fold more potent inhibitor than PPIs, and 6000-fold more potent than H2 receptor antagonists on a molar basis, which allows the expansion and reproduction of H. pylori colonization[18]

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