Correlation between <i>Helicobacter pylori</i> Infection and IL‐18 mRNA Expression in Human Gastric Biopsy Specimens

Fera, M. T.; Carbone, M.; Buda, C.; Aragona, Marcello; Panetta, Stefania; Giannone, M.; Torre, Francesco La; Giudice, Antonino Lo; Losi, E.

doi:10.1111/j.1749-6632.2002.tb04125.x

Cited by 13 publications

(9 citation statements)

References 10 publications

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“…All three cytokines transcript levels were significantly higher in H. pylori-infected children compared with uninfected individuals, and they were associated with the activity of antral inflammation, which supports earlier observations in adults [13,17,19,20]. Earlier studies revealed that expression of IL-1b and IL-8, but not IL-18 is significantly influenced by H. pylori genotype [13,17,21].…”

Section: Discussionsupporting

confidence: 79%

Enhanced gastric IL-18 mRNA expression in Helicobacter pylori-infected children is associated with macrophage infiltration, IL-8, and IL-1β mRNA expression

Dzierżanowska-Fangrat

Michałkiewicz²,

Cielecka-Kuszyk³

et al. 2008

European Journal of Gastroenterology & Hepatology

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Section: Discussionsupporting

confidence: 79%

Enhanced gastric IL-18 mRNA expression in Helicobacter pylori-infected children is associated with macrophage infiltration, IL-8, and IL-1β mRNA expression

Dzierżanowska-Fangrat

Michałkiewicz²,

Cielecka-Kuszyk³

et al. 2008

European Journal of Gastroenterology & Hepatology

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“…Tomita et al (15) reported that antral IL-18 mRNA levels were up-regulated in H. pylori infection, whereas mature IL-18 protein was present in mucosa of both infected and uninfected subjects as measured by immunoblot analyses. In contrast, Fera et al reported that antral H. pylori infection was associated with IL-18 production as determined by immunohistochemistry; whereas IL-18 mRNA was expressed irrespective of H. pylori infection (16). The reason for the discrepancy is unknown; however, one reason might be due to the nonquantitative nature of analyses of mRNA and protein levels.…”

Section: T Hementioning

confidence: 56%

Regulation of IL-18 inHelicobacter pyloriInfection

Yamauchi

Choi

Lü

et al. 2008

The Journal of Immunology

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The gastric mucosal immune response is thought to be comprised predominantly of the Th1 type; however, there are limited data regarding the role of IL-18 in Helicobacter pylori-induced inflammation. We investigated IL-18 levels in gastric mucosal biopsy specimens as well as in isolated gastric epithelial cells and lamina propria mononuclear cells. We also investigated IL-18 levels in gastric epithelial cells and the monocyte cell line THP-1 cocultured with H. pylori. In both systems, IL-18 levels were markedly enhanced in H. pylori-infected epithelial cells and monocytes. IL-18 levels in H. pylori-infected gastric mucosa were well correlated with the severity of gastric inflammation, confirming that H. pylori-induced IL-18 plays an important role in gastric injury. Virulence factors of H. pylori; the cag pathogenicity island and OipA affected IL-18 induction in different manners. Up-regulation of IL-18 mRNA/protein in epithelial cells was dependent on both virulence factors. Interestingly, up-regulation of IL-18 mRNA in monocytes was independent of both factors, whereas IL-18 protein was OipA dependent – cag pathogenicity island independent, indicating that OipA regulates IL-18 induction in monocytes at the posttranscriptional level. IL-18 levels in the gastric biopsy specimens showed similar patterns to those in lamina propria mononuclear cells with respect to virulence factors, suggesting that submucosal monocytes/macrophages are the main source of IL-18 induced by H. pylori infection. H. pylori appeared to regulate the ERK/JNK→AP-1 pathway in both cell types. In addition, OipA and its related p38 pathway may be closely involved in IL-18 induction in H. pylori-infected gastric mucosa and may contribute to gastric injury.

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“…( 19 ) Some studies in humans have reported that IL‐18 protein and/or mRNA levels correlate with the severity of gastric inflammation; ( 18,19 ) however, other studies have reported that IL‐18 mRNA levels are independent of H. pylori infection. ( 45 ) Gastric mucosal IL‐18 levels increased in Mongolian gerbil after H. pylori infection; however, IL‐18 mRNA levels did not correlate with the mRNA levels of IL‐1β, IL‐17, or TNF‐α, or with the degree of inflammatory cell infiltration. There was also no significant difference in IL‐18 mRNA levels between gerbils with gastric ulcer or gastritis.…”

Section: Discussionmentioning

confidence: 88%

Gastric mucosal interleukin‐17 and ‐18 mRNA expression in Helicobacter pylori‐induced Mongolian gerbils

et al. 2009

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Helicobacter pylori infection causes characteristic mucosal infiltration of inflammatory cells, resulting in the development of peptic ulcers and gastric cancer in approximately 10% of cases. Different clinical expressions of the infection may reflect different patterns of cytokine expression. Interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-17, and IL-18 have been reported to be involved in H. pylori-induced gastric mucosal inflammation, but the details and relation to different patterns of inflammation remain unclear. Moreover, the proinflammatory virulence factor outer inflammatry protein (OipA) was reported to be associated with gastric mucosal inflammatory cytokine levels. To clarify these findings, Mongolian gerbils were infected for up to 12 months with wild-type H. pylori 7.13 or with isogenic oipA mutants for 3 months, and mucosal cytokines (IL-1β, IL-17, IL-18, and TNF-α) mRNA levels were then assessed using real-time RT-PCR. Antral mucosal IL-1β and IL-18 mRNA levels peaked 1 month after infection, whereas the peak of TNF-α mRNA was at 6–12 months; IL-17 levels peaked at 12 months. The inflammatory cell infiltration and mRNA levels of all cytokines studied were significantly lower in oipA mutants than in wild-type-infected gerbils. Mucosal IL-1β, IL-17, and TNF-α expression, but not that of IL-18, were significantly associated with the grade of inflammatory cell infiltration. The pattern of increased inflammatory cytokines differed relative to the phase of the infection and pattern of inflammation. OipA appears to play a role in IL-1β, IL-17, and TNF-α expression and the resulting inflammation.

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Correlation between Helicobacter pylori Infection and IL‐18 mRNA Expression in Human Gastric Biopsy Specimens

Abstract: Our data indicate that H. pylori infection is associated with active interleukin‐18 production in patients with chronic gastritis. Different cell types appear to be involved in this activity and may play a role in the development of immunopathologic damage.

Cited by 13 publications

References 10 publications

Enhanced gastric IL-18 mRNA expression in Helicobacter pylori-infected children is associated with macrophage infiltration, IL-8, and IL-1β mRNA expression

Enhanced gastric IL-18 mRNA expression in Helicobacter pylori-infected children is associated with macrophage infiltration, IL-8, and IL-1β mRNA expression

Regulation of IL-18 inHelicobacter pyloriInfection

Gastric mucosal interleukin‐17 and ‐18 mRNA expression in Helicobacter pylori‐induced Mongolian gerbils

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