Relationship of IL-1 and TNF-α polymorphisms with Helicobacter pylori in gastric diseases in a Brazilian population

Abstract

It is well known that the risk of development of gastric cancer (GC) in Helicobacter pylori -infected patients depends on several factors. Thus, the aim of this study was to investigate the effect of proinflammatory cytokine gene polymorphisms for IL-1β , IL-1RN and TNF-α on the development of GC in a Brazilian population. A total of 202 biopsies obtained from Brazilian patients with chronic gastritis and GC were included in the study. Infection with H. pylori cag A + was determined by the polymerase chain reaction (PCR) as previously described. IL-1β , IL-1RN and TNF-α polymorphism genotyping was performed by restriction fragment length polymorphism PCR. Associations between gene polymorphisms, clinical diseases and virulence markers were evaluated using either the X 2 test or the Fisher exact test. Our results demonstrated that the IL-1β -511 C/C and IL-1β -511 C/T alleles were associated with chronic gastritis in H. pylori -positive patients (P = 0.04 and P = 0.05, respectively) and the IL-1β -511 C/C genotype was associated with GC (P = 0.03). The frequency of IL-1RN alleles from patients with chronic gastritis and GC indicated that there was no difference between the genotypes of the groups studied. Similar results were found for TNF-α -308 gene polymorphisms. Our results indicate that the IL-1β -511 C/C and C/T gene polymorphisms are associated with chronic gastritis and GC development in H. pylori -infected individuals.

Osteopontin depletion decreases inflammation and gastric epithelial proliferation during Helicobacter pylori infection in mice

“…25,26 Notably, there is considerable evidence that elevated expression of IL-1β, IFN-γ, and TNF-α are associated with chronic gastritis and gastric cancer development following HP infection. 7,11,25,27,28 Our study revealed that OPN expression was elevated in response to HP infection, and OPN depletion decreased production of these cytokines in both gastric epithelial cells and macrophages during HP infection. These results suggest that OPN is an important mediator of proinflammatory cytokine production during HP infection.…”

Цитокіновий Статус У дітей Із хронічною Гастродуоденальною Патологією

“…Зокрема, інтерлейкін-4 (IL-4) є клю-човим медіатором Th2-типу імунної відповіді, який має протизапальні властивості, стимулює проліфе-рацію В-клітин, синтез IgE, базофілів, пригнічує синтез прозапальних цитокінів та цитотоксичність Т-клітин і макрофагів, відіграє роль при алергічному запаленні та протигельмінтному захисті [6]. Фактор некрозу пухлини альфа (TNF-) має прозапальні властивості, є важливим ендогенним пірогенним фактором, сприяє проліферації лімфоцитів, акти-вує макрофаги і натуральні кілери, сприяє синтезу прозапальних цитокінів [7,8]. Недостатньо вивчена і потребує подальшого дослідження участь паразитів в етіології та патогенезі різних захворювань травної системи.…”

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

“…IL-1 is a powerful inhibitor of gastric acid secretion; on a molar basis, IL-1 is estimated to be 100-fold more potent than proton pump inhibitors and 6000-fold more potent than H 2 receptor antagonists [16,40,41]. The decrease of the acid secretion causes hypochlorhydria, which favors H. pylori infection because the secretion of acid is an important host defense mechanism against bacterial colonization in the stomach.…”

“…IL-1, a powerful inhibitor of gastric acid secretion, is up-regulated in the presence of H. pylori and plays a major role in initiating and amplifying the inflammatory response to this infection [3,16]. Three single nucleotide polymorphisms (SNPs) associated with high levels of IL-1 secretion have been reported in the IL-1B gene: a T-C base transition at position -31 and C-T base transitions at positions -511 and +3954 from the transcriptional start site [17][18][19].…”