<i>Helicobacter pylori</i> Stimulates a Mixed Adaptive Immune Response with a Strong T‐Regulatory Component in Human Gastric Mucosa

Goll, Rasmus; Gruber, Franz; Olsen, Trine; Cui, Guanglin; Raschpichler, Gabriele; Buset, Magne; Asfeldt, Anne Mette; Husebekk, Anne; Florholmen, Jon

doi:10.1111/j.1523-5378.2007.00495.x

Cited by 64 publications

(74 citation statements)

References 42 publications

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“…They further showed that people with ulcers had reduced Treg responses and increased Th1 and Th2 responses compared with those without ulcers. These studies suggest a protective role for TGF-␤ and Tregs, but there are also some studies indicating that Tregs induced during H. pylori infection may promote prolonged infection, and these studies lend support to the notion that Tregs are important in the chronicity of infection (12). Another group demonstrated that memory T cells from infected individuals did not respond well to H. pylori membrane preparations compared to memory cells from uninfected individuals, but the activity was restored in infected individuals when Tregs were depleted (24).…”

Section: Discussionmentioning

confidence: 61%

Role of Gastric Epithelial Cell-Derived Transforming Growth Factor β in Reduced CD4 ⁺ T Cell Proliferation and Development of Regulatory T Cells during Helicobacter pylori Infection

et al. 2011

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Section: Discussionmentioning

confidence: 61%

Role of Gastric Epithelial Cell-Derived Transforming Growth Factor β in Reduced CD4 ⁺ T Cell Proliferation and Development of Regulatory T Cells during Helicobacter pylori Infection

et al. 2011

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“…It has become clear that hosts that mount a strong proinflammatory response are more likely to develop severe complications of disease, such as peptic ulcers or neoplasia (17), although the factors that determine which hosts will develop such responses remain unclear. In fact, the most recent evidence suggests that in humans, the primary response to infection is actually immunoregulatory (18)(19)(20)(21)(22). This finding supports many years of animal research indicating that suppression of regulatory responses is necessary for induction of severe disease (11,(23)(24)(25)(26)(27)(28)(29)(30)(31).…”

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confidence: 53%

Complex T Cell Interactions Contribute to Helicobacter pylori Gastritis in Mice

et al. 2013

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Disease due to the gastric pathogen Helicobacter pylori varies in severity from asymptomatic to peptic ulcer disease and cancer. Accumulating evidence suggests that one source of this variation is an abnormal host response. The goal of this study was to use a mouse model of H. pylori gastritis to investigate the roles of regulatory T cells (Treg) as well as proinflammatory T cells (Th1 and Th17) in gastritis, gastric T cell engraftment, and gastric cytokine production. Our results support published data indicating that severe gastritis in T cell recipient mice is due to failure of Treg engraftment, that Treg ameliorate gastritis, and that the proinflammatory response is attributable to interactions between several cell subsets and cytokines. We confirmed that gamma interferon (IFN-␥) is essential for induction of gastritis but showed that IFN-␥-producing CD4 T cells are not necessary. Interleukin 17A (IL-17A) also contributed to gastritis, but to a lesser extent than IFN-␥. Tumor necrosis factor alpha (TNF-␣) and IL-17F were also elevated in association with disease. These results indicate that while H. pylori-specific CD4 ؉ T cells and IFN-␥ are both essential for induction of gastritis due to H. pylori, IFN-␥ production by T cells is not essential. It is likely that other proinflammatory cytokines, such as IL-17F and TNF-␣, shown to be elevated in this model, also contribute to the induction of disease. We suggest that gastritis due to H. pylori is associated with loss of immunoregulation and alteration of several cytokines and cell subsets and cannot be attributed to a single immune pathway.

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“…IL-1β have a major role in the initiation of the host immune response against H. pylori infections. The mRNA expression of IL-1β was shown to increase in patients (28)(29)(30). In addition to IL-1β, the inflammatory cells also secrete TNF-α during H. pylori-induced inflammation (31).…”

Section: Discussionmentioning

confidence: 98%

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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Helicobacter pylori Stimulates a Mixed Adaptive Immune Response with a Strong T‐Regulatory Component in Human Gastric Mucosa

Abstract: The cytokine profile of H. pylori-infected gastric mucosa shows a mixed Th1-Th2 profile. Furthermore, a high IL10 expression may indicate that also regulatory T cells play a role in the chronic phase of H. pylori infection.

Cited by 64 publications

References 42 publications

Role of Gastric Epithelial Cell-Derived Transforming Growth Factor β in Reduced CD4 ⁺ T Cell Proliferation and Development of Regulatory T Cells during Helicobacter pylori Infection

Role of Gastric Epithelial Cell-Derived Transforming Growth Factor β in Reduced CD4 ⁺ T Cell Proliferation and Development of Regulatory T Cells during Helicobacter pylori Infection

Complex T Cell Interactions Contribute to Helicobacter pylori Gastritis in Mice

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

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Helicobacter pylori Stimulates a Mixed Adaptive Immune Response with a Strong T‐Regulatory Component in Human Gastric Mucosa

Abstract: The cytokine profile of H. pylori-infected gastric mucosa shows a mixed Th1-Th2 profile. Furthermore, a high IL10 expression may indicate that also regulatory T cells play a role in the chronic phase of H. pylori infection.

Cited by 64 publications

References 42 publications

Role of Gastric Epithelial Cell-Derived Transforming Growth Factor β in Reduced CD4 + T Cell Proliferation and Development of Regulatory T Cells during Helicobacter pylori Infection

Role of Gastric Epithelial Cell-Derived Transforming Growth Factor β in Reduced CD4 + T Cell Proliferation and Development of Regulatory T Cells during Helicobacter pylori Infection

Complex T Cell Interactions Contribute to Helicobacter pylori Gastritis in Mice

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

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Product

Resources

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Role of Gastric Epithelial Cell-Derived Transforming Growth Factor β in Reduced CD4 ⁺ T Cell Proliferation and Development of Regulatory T Cells during Helicobacter pylori Infection

Role of Gastric Epithelial Cell-Derived Transforming Growth Factor β in Reduced CD4 ⁺ T Cell Proliferation and Development of Regulatory T Cells during Helicobacter pylori Infection