Relevance of IL-1 and TNF gene polymorphisms on interleukin-1β and tumor necrosis factor-α gastric mucosal production

García-González, María Asunción; Aísa, M.A. Pérez; Strunk, Mark; Benito, Rafael; Piazuelo, Elena; Jiménez, Pilar; Sopeña, Federico; Lanas, Ángel

doi:10.1016/j.humimm.2009.07.024

Cited by 24 publications

(11 citation statements)

References 57 publications

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“…The frequencies of polymorphisms in the IL-1B and IL-1RN genes found in this study were similar to those described in European populations [37,38]. Genetic polymorphisms involved in the regulation of gastric acid secretion may to be associated with host susceptibility to the acquisition of H. pylori infection and to the development of gastric pathologies [18,36].…”

Section: Discussionsupporting

confidence: 86%

Relationship of interleukin-1B gene promoter region polymorphism with Helicobacter pylori infection and gastritis

Ramis

Vianna

Halicki

et al. 2015

J Infect Dev Ctries

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Introduction: Helicobacter pylori infection is associated with gastritis, peptic ulcer disease and gastric carcinoma. The severity of damage is determined by the interplay between environmental/behavioral factors, bacterial pathogenicity genes and host genetic polymorphisms that can influence the secretion levels of inflammatory cytokines. Accordingly, this study aimed to identify polymorphisms in the IL-1B and IL-1RN genes and their associations with H. pylori infection, cagA gene of H. pylori, and gastroduodenal diseases.

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Section: Discussionsupporting

confidence: 86%

Relationship of interleukin-1B gene promoter region polymorphism with Helicobacter pylori infection and gastritis

Ramis

Vianna

Halicki

et al. 2015

J Infect Dev Ctries

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“…Previous studies have found that the IL-1Ra/IL-1 ratio is influenced by genetic variations in IL1RN (Barlo et al 2011; Carter et al 2004). Higher IL-1 protein levels were found in gastric mucosa from Helicobacter pylori -infected individuals that carried VNTR*2 (Garcia-Gonzalez et al 2009), while lower IL-Ra protein levels were found in biopsies from ulcerative colitis patients with VNTR*2 (Carter et al 2004). Together, this indicates that carriers of VNTR*2 have low levels of IL-1Ra but higher IL-1 levels.…”

Section: Discussionmentioning

confidence: 99%

IL1RN genetic variations and risk of IPF: a meta-analysis and mRNA expression study

et al. 2012

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Idiopathic pulmonary fibrosis (IPF) is a rare and devastating lung disease of unknown aetiology. Genetic variations in the IL1RN gene, encoding the interleukin-1 receptor antagonist (IL-1Ra), have been associated with IPF susceptibility. Several studies investigated the variable number tandem repeat (VNTR) or single nucleotide polymorphisms rs408392, rs419598 and rs2637988, with variable results. The aim of this study was to elucidate the influence of polymorphisms in IL1RN on IPF susceptibility and mRNA expression. We performed a meta-analysis of the five case–control studies that investigated an IL1RN polymorphism in IPF in a Caucasian population. In addition, we investigated whether IL1RN mRNA expression was influenced by IL1RN polymorphisms. The VNTR, rs408392 and rs419598 were in tight linkage disequilibrium, with D′ > 0.99. Furthermore, rs2637988 was in linkage disequilibrium with the VNTR (D′ = 0.90). A haploblock of VNTR*2 and the minor alleles of rs408392and rs419598 was constructed. Meta-analysis revealed that this VNTR*2 haploblock is associated with IPF susceptibility both with an allelic model (odds ratio = 1.42, p = 0.002) and a carriership model (odds ratio = 1.60, p = 0.002). IL1RN mRNA expression was significantly influenced by rs2637988, with lower levels found in carriers of the (minor) GG genotype (p < 0.001). From this meta-analysis, we conclude that the VNTR*2 haploblock is associated with susceptibility to IPF. In addition, polymorphisms in IL1RN influence IL-1Ra mRNA expression, suggesting that lower levels of IL-1Ra predispose to developing IPF. Together these findings demonstrate that the cytokine IL-1Ra plays a role in IPF pathogenesis.

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“…For example, the gastric mucosa of H. pylori-infected patients has increased levels of proinflammatory cytokines such as IL-8 and TNF-␣ (8,13,22,40). IL-8 and TNF-␣ have a central role in the modification of the cellular microenvironment (4,30,40).…”

Section: Discussionmentioning

confidence: 99%

Peptidoglycan Deacetylation in Helicobacter pylori Contributes to Bacterial Survival by Mitigating Host Immune Responses

Wang

Maier

et al. 2010

Infect Immun

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An oxidative stress-induced enzyme, peptidoglycan deacetylase (PgdA), in the human gastric pathogen Helicobacter pylori was previously identified and characterized. In this study, we constructed H. pylori pgdA mutants in two mouse-adapted strains, X47 and B128, to investigate the role of PgdA in vivo (to determine the mutants' abilities to colonize mice and to induce an immune response). H. pylori pgdA mutant cells showed increased sensitivity to lysozyme compared to the sensitivities of the parent strains. We demonstrated that the expression of PgdA was significantly induced (3.5-fold) when H. pylori cells were in contact with macrophages, similar to the effect observed with oxidative stress as the environmental inducer. Using a mouse infection model, we first examined the mouse colonization ability of an H. pylori pgdA mutant in X47, a strain deficient in the major pathway (cag pathogenicity island [PAI] encoded) for delivery of peptidoglycan into host cells. No animal colonization difference between the wild type and the mutant was observed 3 weeks after inoculation. However, the pgdA mutant showed a significantly attenuated ability to colonize mouse stomachs (9-fold-lower bacterial load) at 9 weeks postinoculation. With the cag PAI-positive strain B128, a significant colonization difference between the wild type and the pgdA mutant was observed at 3 weeks postinoculation (1.32 ؋ 10 4 versus 1.85 ؋ 10 3 CFU/gram of stomach). To monitor the immune responses elicited by H. pylori in the mouse infection model, we determined the concentrations of cytokines present in mouse sera. In the mice infected with the pgdA mutant strain, we observed a highly significant increase in the level of MIP-2. In addition, significant increases in interleukin-10 and tumor necrosis factor alpha in the pgdA mutant-infected mice compared to the levels in the wild-type H. pylori-infected mice were also observed. These results indicated that H. pylori peptidoglycan deacetylation is an important mechanism for mitigating host immune detection; this likely contributes to pathogen persistence.

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Relevance of IL-1 and TNF gene polymorphisms on interleukin-1β and tumor necrosis factor-α gastric mucosal production

Cited by 24 publications

References 57 publications

Relationship of interleukin-1B gene promoter region polymorphism with Helicobacter pylori infection and gastritis

Relationship of interleukin-1B gene promoter region polymorphism with Helicobacter pylori infection and gastritis

IL1RN genetic variations and risk of IPF: a meta-analysis and mRNA expression study

Peptidoglycan Deacetylation in Helicobacter pylori Contributes to Bacterial Survival by Mitigating Host Immune Responses

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