Levels of Interleukin‐18 Are Markedly Increased in<i>Helicobacter pylori</i>–Infected Gastric Mucosa among Patients with Specific<i>IL18</i>Genotypes1

Sakai, Kyoko; Kita, Masakazu; Sawai, Naoki; Shiomi, Satoshi; Sumida, Yoshio; Kanemasa, Kazuyuki; Mitsufuji, Shoji; Imanishi, Jirô; Yamaoka, Yoshio

doi:10.1086/588196

Cited by 26 publications

(46 citation statements)

References 39 publications

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“…Similar to our results there were reports indicating no increase in IL-12 secretion. Sakai et al (43) showed that there was no increase in the IL-12 secretion of the gastric mucosa Therefore, although we had limited number of strains in this study, it is important to note that this is the first study performed in Turkey. As conclusion, we suggest that the severity of host immune response may differ due to the different types of H. pylori strains.…”

Section: Discussionmentioning

confidence: 84%

The cytokine response in THP-1 (monocyte) and HL-60 (neutrophil-differentiated) cells infected with different genotypes of Helicobacter pylori strains

Caliskan

Sayi-Yazgan²,

Tokman³

et al. 2015

Turk J Gastroenterol

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Background/Aims: Helicobacter pylori (H. pylori) is a microaerophilic bacterium related with peptic ulcer and gastric cancer. Its virulence factors include cytotoxin-associated gene A (CagA) and vacuolating cytotoxin gene A (VacA) proteins. Cytokine release inducted by H. pylori colonization has an important role in pathogenesis of H. pylori. The severity of gastric pathologies depends on the H. pylori genotypes found in different geographical regions. We aimed to determine the relationship between different H. pylori genotypes and their effects on the cytokine release levels. Materials and Methods: ureC, cagA, vacAs1/s2, vacAm1/m2, and blood group antigen-binding adhesion protein A2 (babA2) virulence related genes were investigated in 21 H. pylori strains. Genotyping of 21 strains were made due to the presence of cagA, vacAs1/s2, vacAm1/m2, and babA2 genes. The H. pylori strains were cultured together with THP-1 and neutrophil-differentiated Human promyelocytic leukemia cells (HL-60) cells. The levels of cytokines interleukin (IL)-1β, IL-6, IL-8, IL-12, tumor necrosis factor-alpha (TNF-α), and IL-10 in these cells were measured after co-culturing with H. pylori strains. Results: The following five different genotypes were detected: Genotype1: cagA and vacAs1m2; Genotype2: cagA and vacAs1m1; Genotype3: cagA, vacAs1m2, and babA2; Genotype4: vacAs2m2; and Genotype5: cagA and vacAs2m2. All these genotypes significantly induced the levels of IL-1β, IL-6, IL-8, IL 10, and TNF-α in THP-1 cells. Genotype 5 caused higher amounts of IL-1β, IL-6, TNF-α, and IL-10, whereas genotype 1 induced the highest levels of IL-8. In neutrophil-differentiated HL-60 cells, genotype 4 increased IL-6 levels and genotype 3 and 4 elevated IL-8 levels significantly. Conclusion: These results suggested that cytokine response of the host varies depending on the specific immune response of the host against different H. pylori strains.

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Section: Discussionmentioning

confidence: 84%

The cytokine response in THP-1 (monocyte) and HL-60 (neutrophil-differentiated) cells infected with different genotypes of Helicobacter pylori strains

Caliskan

Sayi-Yazgan²,

Tokman³

et al. 2015

Turk J Gastroenterol

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“…An increased IL-18 expression has been reported in human atherosclerotic plaques 100) , and animal models further support the proatherogenic role of IL-18 101) and beneficial effects of IL-18 inhibition on plaque progression and composition 102) . In particular, several epidemiologic studies have reported that H. pylori infection upregulates IL-18 production from human gastric epithelial cells and lamina propria mononuclear cells isolated from H. pylori-infected gastric mucosa [103][104][105] . Furthermore, the serum H. pylori-IgG level is positively correlated with the serum IL-18 level 81) , and the IL-18 level is influenced by CagA-positive H. pylori strains 106) .…”

Section: H Pylori and Endothelial Dysfunctionmentioning

confidence: 99%

Helicobacter pylori—An Infectious Risk Factor for Atherosclerosis?

Yang

Lü

2014

JAT

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Accumulating evidence implicates Helicobacter pylori (H. pylori) infection in the pathogenesis of certain diseases localized outside the stomach, particularly those characterized by persistent and lowgrade systematic inflammation. Recently, the role of H. pylori infection in the development of atherosclerosis and its clinical complications has received attention. Atherosclerosis is a high-cost disease, and acute events resulting from this condition rank first among morbidity and mortality statistics in most industrialized countries. Atherosclerosis is a multifactorial disorder, and traditional risk factors explain only 50% of its etiology. Therefore, identifying new risk factors for atherosclerosis is necessary. Serological studies indicate that chronic H. pylori infection, especially that with more virulent strains, may predispose patients to the onset of atherosclerosis and related adverse clinical events, and PCR studies have detected H. pylori DNA in atherosclerotic plaques, although this finding remains controversial. If this association were to be confirmed, its importance to public health would be substantial, as the eradication of H. pylori is more straightforward and less costly than the longterm treatment of other risk factors. This review investigates the potential relationship between H. pylori infection and atherosclerosis from both epidemiological and pathogenic perspectives and characterizes the potential mechanisms underlying this correlation.

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“…The signature cytokines of T H 1-polarized cellular immune responses, IFN-␥, IL-12, and IL-18, are also present at elevated levels (26,27). Despite the production of large amounts of both types of cytokines and the efficient recruitment of neutrophil granulocytes, macrophages, and various lymphocyte populations to the site of infection, the immune response of the host is typically inadequate to clear the infection.…”

mentioning

confidence: 99%

The CD4+ T Cell-Mediated IFN-γ Response to Helicobacter Infection Is Essential for Clearance and Determines Gastric Cancer Risk

Sayi

Kohler

Hitzler

et al. 2009

The Journal of Immunology

153

184

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Levels of Interleukin‐18 Are Markedly Increased inHelicobacter pylori–Infected Gastric Mucosa among Patients with SpecificIL18Genotypes1

Abstract: H. pylori infection induces IL-18 in the gastric mucosa. H. pylori-infected patients with IL18 -607C/C and -137G/G have higher IL-18 levels, which causes severe gastric inflammation. IL18 genotype might be a marker for predicting the effects of eradication therapy.

Cited by 26 publications

References 39 publications

The cytokine response in THP-1 (monocyte) and HL-60 (neutrophil-differentiated) cells infected with different genotypes of Helicobacter pylori strains

The cytokine response in THP-1 (monocyte) and HL-60 (neutrophil-differentiated) cells infected with different genotypes of Helicobacter pylori strains

Helicobacter pylori—An Infectious Risk Factor for Atherosclerosis?

The CD4+ T Cell-Mediated IFN-γ Response to Helicobacter Infection Is Essential for Clearance and Determines Gastric Cancer Risk

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