Gene polymorphism of interleukin 1 and 8 in chronic gastritis patients infected with Helicobacter pylori

Neto, Agostinho Caleman; Rasmussen, Lucas Trevizani; Labio, Roger Willian de; Queiroz, V. F.; Smith, Marília de Arruda Cardoso; Viani, Gustavo Arruda; Payão, Spencer L.M.

doi:10.1186/1678-9199-20-17

Cited by 23 publications

(15 citation statements)

References 25 publications

(37 reference statements)

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“…For IL-1B-511C/T, sixteen studies with 2486 cases and 1989 controls concerning IL-1B-511C/T gene polymorphisms were identified [15,24,37–39,41,44,45,48–54]. Overall, there is no significant difference in IL-1B-511C/T genotype distribution between H .…”

Section: Resultsmentioning

confidence: 99%

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

et al. 2017

PLoS ONE

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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

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“…Evidence suggests that the main pathophysiological event in the H. pylori infection of gastric mucosa is the induction of a gastric mucosal inflammatory response. This reaction is induced by the contact of H. pylori with gastric cells, and is followed by neutrophil and mononuclear cell activation and the transcription and synthesis of pro-inflammatory and anti-inflammatory cytokines [ 4 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

Lack of association among TNF-α gene expression, -308 polymorphism (G > A) and virulence markers of Helicobacter pylori

Zabaglia¹,

Ferraz²,

Pereira³

et al. 2015

J Venom Anim Toxins Incl Trop Dis

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BackgroundTumor necrosis factor plays a critical role in the pathogenesis of gastric diseases such as gastric cancer, and an abnormal inflammatory response has frequently been observed in dyspeptic patients. Helicobacter pylori infection can induce a gastric mucosal inflammatory response that may be influenced by -308 (G > A) polymorphisms and gene expression of the TNF-α gene.MethodsOne hundred and thirty-four gastric biopsy samples were collected from patients of both genders (61♂ and 73♀, mean age 40.3 ± 24.2 years) with gastric symptoms. The -308 (G > A) polymorphism of TNF-α was characterized using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). The expression level was measured using real-time PCR, and relative quantification (RQ) was calculated using the comparative CT method (2-ΔΔCT).ResultsThe analysis revealed an increase in TNF-α gene expression in patients with gastritis; on the other hand, no statistical differences were observed in patients with gastric cancer. In addition, no association was found among -308 polymorphism genotypes, virulence markers, or TNF-α gene expression.ConclusionsHelicobacter pylori induces a large increase in TNF-α expression in patients with gastritis, regardless of tissue inflammation, but after the tissue becomes neoplastic, the presence of bacteria did not influence expression. These results suggest that the TNF-α pathway may play an important role in the progression from gastritis to gastric cancer

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“…[ 36 ] The distribution of IL-1β-31 polymorphism genotype differed significantly between H pylori infected patients and the noninfected group, with frequency of TT genotype lower in the former group. [ 6 ]…”

Section: Discussionmentioning

confidence: 99%

Association between IL-1β polymorphisms and gastritis risk

Sun

Cai²,

Li³

et al. 2017

Medicine

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“…Caleman Neto et al[210], have suggested that the IL-1B -31T/T polymorphism acts as a protective factor against H. pylori infection in the Brazilian population.…”

Section: Inflammation Driven Malignancy Riskmentioning

confidence: 99%

Host pathogen interactions in Helicobacter pylori related gastric cancer

Chmiela

Karwowska

Gonciarz

et al. 2017

WJG

125

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Helicobacter pylori (H. pylori), discovered in 1982, is a microaerophilic, spiral-shaped gram-negative bacterium that is able to colonize the human stomach. Nearly half of the world's population is infected by this pathogen. Its ability to induce gastritis, peptic ulcers, gastric cancer and mucosa-associated lymphoid tissue lymphoma has been confirmed. The susceptibility of an individual to these clinical outcomes is multifactorial and depends on H. pylori virulence, environmental factors, the genetic susceptibility of the host and the reactivity of the host immune system. Despite the host immune response, H. pylori infection can be difficult to eradicate. H. pylori is categorized as a group I carcinogen since this bacterium is responsible for the highest rate of cancer-related deaths worldwide. Early detection of cancer can be lifesaving. The 5-year survival rate for gastric cancer patients diagnosed in the early stages is nearly 90%. Gastric cancer is asymptomatic in the early stages but always progresses over time and begins to cause symptoms when untreated. In 97% of stomach cancer cases, cancer cells metastasize to other organs. H. pylori infection is responsible for nearly 60% of the intestinal-type gastric cancer cases but also influences the development of diffuse gastric cancer. The host genetic susceptibility depends on polymorphisms of genes involved in H. pylori-related inflammation and the cytokine response of gastric epithelial and immune cells. H. pylori strains differ in their ability to induce a deleterious inflammatory response. H. pylori-driven cytokines accelerate the inflammatory response and promote malignancy. Chronic H. pylori infection induces genetic instability in gastric epithelial cells and affects the DNA damage repair systems. Therefore, H. pylori infection should always be considered a pro-cancerous factor.

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“…Fabris et al [21] also failed to find any significant association between the IL-8-251 T>A polymorphism and H. pylori infection in Brazilian patients. However, Caleman Neto et al [15] studied adult gastric patients in Brazil and found a significant difference between the TA and TT genotypes in terms of H. pylori presence; however, no correlation was found between the AA genotype and the occurrence of H. pylori . Their results suggest that the presence of the TA genotype may be a risk factor for H. pylori infection whereas the TT genotype may act as a protective factor against H. pylori .…”

Section: Introductionmentioning

confidence: 99%

Interleukin 8 (-251 T>A) polymorphism in children and teenagers infected with Helicobacter pylori

Saes

Labio

Rasmussen

et al. 2017

J Venom Anim Toxins Incl Trop Dis

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Background Helicobacter pylori (H. pylori) is a gram-negative bacterium that colonizes the human stomach and causes a variety of gastric diseases. This study evaluated the correlations between the -251 (T>A) (rs4073) polymorphism of interleukin-8 (IL-8), the etiology of gastric disease, and H. pylori infection in pediatric and adolescent patients.MethodsDNA samples were obtained from 285 gastric biopsies from pediatric patients. H. pylori was detected by PCR, whereas PCR-RFLP was used to characterize the -251 (T>A) polymorphism of IL-8.ResultsThe histological analysis revealed the presence of gastritis in 158 patients (55.44%). H. pylori was found in 71 samples (24.9%). The -251 (T>A) polymorphism revealed that 58 (29.47%) samples were TT, 143 (50.18%) samples were TA, and 84 (20.35%) samples were AA.ConclusionsOur findings suggest that IL8-251 A allele may be an important risk factor for the development of gastric disease when associated with H. pylori infection.

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Gene polymorphism of interleukin 1 and 8 in chronic gastritis patients infected with Helicobacter pylori

Cited by 23 publications

References 25 publications

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

Lack of association among TNF-α gene expression, -308 polymorphism (G > A) and virulence markers of Helicobacter pylori

Association between IL-1β polymorphisms and gastritis risk

Host pathogen interactions in Helicobacter pylori related gastric cancer

Interleukin 8 (-251 T>A) polymorphism in children and teenagers infected with Helicobacter pylori

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