Implications for a role of interleukin-23 in the pathogenesis of chronic gastritis and of peptic ulcer disease

Koussoulas, Vassilios; Vassiliou, Spyridon; Giamarellos‐Bourboulis, Evangelos J.; Tassias, G; Kotsaki, Antigone; Tzivras, Michalis

doi:10.1111/j.1365-2249.2008.03859.x

Cited by 13 publications

(16 citation statements)

References 17 publications

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“…IL‐23 and IL‐1ß levels in the supernatants of the samples of gastric mucosa, taken from patients with duodenal ulcers, with gastric ulcers and with chronic gastritis, were higher among the H. pylori ‐positive patients, as compared with the H. pylori ‐negative patients . In a recent study, increased IL‐23, IL‐6, and TGF‐β cytokines were observed in the culture‐containing macrophage cells stimulated with H. pylori antigen, followed by the activation of Th17, and the secretion of IL‐17 .…”

Section: Discussionsupporting

confidence: 72%

“…In addition to evaluating the serum levels of IL-17A, IL-21, IL-22, IL-23, and TGF-b, and their differences in the above-mentioned patients, we also evaluated the levels of these cytokines in the same groups of patients through stimulating the PBMCs by H. pylori antigen, PHA, or anti-CD3/CD28. IL-23 and IL-1ß levels in the supernatants of the samples of gastric mucosa, taken from patients with duodenal ulcers, with gastric ulcers and with chronic gastritis, were higher among the H. pylori -positive patients, as compared with the H. pylori -negative patients [35]. In a recent study, increased IL-23, IL-6, and TGF-b cytokines were observed in the culture-containing macrophage cells stimulated with H. pylori antigen, followed by the activation of Th17, and the secretion of IL-17 [46].…”

Section: Discussionmentioning

confidence: 85%

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Alterations in Th17 and the Respective Cytokine Levels in Helicobacter pylori‐Induced Stomach Diseases

et al. 2015

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Section: Discussionsupporting

confidence: 72%

Section: Discussionmentioning

confidence: 85%

Alterations in Th17 and the Respective Cytokine Levels in Helicobacter pylori‐Induced Stomach Diseases

et al. 2015

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“…23 Similarly, in the current study we observed in- Knowing the fact that, naïve CD4-positive T-cell differentiation into Th22 is regulated by IL6 and TNFα, and promoted by IL1β. Therefore, overactivity of these cells and a shift in favor of pro-inflammatory cytokines may lead to gastric ulcers.…”

Section: In Vitro Cytokine Production By Pbmcs Stimulated With H Psupporting

confidence: 80%

“…Koussoulas and Shamsdin determinedthat IL-23 might play a critical role in the process of inflammation and contribution to gastritis 19,23. Koussoulas and Shamsdin determinedthat IL-23 might play a critical role in the process of inflammation and contribution to gastritis 19,23.…”

mentioning

confidence: 99%

The importance of TH22 and TC22 cells in the pathogenesis of Helicobacter pylori‐associated gastric diseases

et al. 2016

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“…However, positive correlations were found between levels of IL-23 and the degree of infiltration of neutrophils and monocytes in patients with H. pylori infection, and the kinetics of IL-23 expression correlates with those of IL-1β (Koussoulas et al, 2009). …”

Section: Introductionmentioning

confidence: 99%

IL-23 Contributes to Control of Chronic Helicobacter Pylori Infection and the Development of T Helper Responses in a Mouse Model1

Horvath¹,

Washington²,

Cope³

et al. 2012

Front. Immun.

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The immune response to Helicobacter pylori involves a mixed T helper-1, T helper-2, and T helper-17 response. It has been suggested that T helper cells contribute to the gastric inflammatory response during infection, and that T helper 1 (Th1) and T helper 17 (Th17) subsets may be required for control of H. pylori colonization in the stomach. The relative contributions of these subsets to gastritis and control of infection are still under investigation. IL-23 plays a role in stabilizing and expanding Th17 cell cytokine expression. Expression of IL-23, which is induced in dendritic cells and macrophages following co-culture with H. pylori, has also been reported to increase during H. pylori infection in humans and animal models. To investigate the role of IL-23 in H. pylori, we infected IL-23p19 deficient mice (IL-23−/−) and wild-type littermates with H. pylori strain SS1. At various time points post-infection, we assessed colonization, gastric inflammation, and cytokine profiles in the gastric tissue. Specifically, H. pylori-infected IL-23−/− mice have higher levels of H. pylori in their stomachs, significantly less chronic gastritis, and reduced expression of IL-17 and IFNγ compared to H. pylori-infected wild-type mice. While many of these differences were significant, the H. pylori infected IL-23−/− had mild increases in our measurements of disease severity. Our results indicate that IL-23 plays a role in the activation of the immune response and induction of gastritis in response to H. pylori by contributing to the control of infection and severity of gastritis.

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Implications for a role of interleukin-23 in the pathogenesis of chronic gastritis and of peptic ulcer disease

Abstract: SummaryThe present study aimed to investigate the role of gastric mucosa for the secretion of interleukin (

Cited by 13 publications

References 17 publications

Alterations in Th17 and the Respective Cytokine Levels in Helicobacter pylori‐Induced Stomach Diseases

Alterations in Th17 and the Respective Cytokine Levels in Helicobacter pylori‐Induced Stomach Diseases

The importance of TH22 and TC22 cells in the pathogenesis of Helicobacter pylori‐associated gastric diseases

IL-23 Contributes to Control of Chronic Helicobacter Pylori Infection and the Development of T Helper Responses in a Mouse Model1

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