Cytokine gene expression in Helicobacter pylori associated antral gastritis.

Moss, Steven F.; Legon, S.; Davies, J.; Calam, J.

doi:10.1136/gut.35.11.1567

Cited by 179 publications

(127 citation statements)

References 20 publications

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“…In our study, however, neither CRP nor WBC was different between AG-positive and AG-negative groups. Nevertheless, mucosal inflammation of the stomach may have influenced arterial stiffness in our subjects, because PG has been regarded as a marker of inflammation of the gastric mucosa as well as gastric atrophy 40) , Other pro-inflammatory cytokines, such as tumor necrosis factor and IL-6, which are closely associated with both HP infection 41) and atherosclerosis 42) , are also candidates, which may explain our findings. It thus seems likely that AG caused by HP, but not HP per se, is one of the risk factors for atherosclerosis; however, the difference in metabolic parameters does not seem to explain completely the difference in arterial stiffness between AG-positive and AG-negative groups.…”

Section: Discussionsupporting

confidence: 57%

Possible Association of Atrophic Gastritis and Arterial Stiffness in Healthy Middle-Aged Japanese

Torisu

Takata

Ansai

et al. 2009

JAT

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Aim: Helicobacter pylori (HP) has been implicated as a risk factor for cardiovascular and atherosclerotic diseases. Arterial stiffness determined by pulse wave velocity (PWV) or the cardio-ankle vascular index (CAVI) has been shown to be higher in HP-positive subjects than in HP-negative subjects; however, this result has been observed only in young subjects. The aim of the study was to investigate the possible correlation between HP infection and PWV or CAVI in middle-aged subjects.

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Section: Discussionsupporting

confidence: 57%

Possible Association of Atrophic Gastritis and Arterial Stiffness in Healthy Middle-Aged Japanese

Torisu

Takata

Ansai

et al. 2009

JAT

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“…IL-8 mRNA/18SrRNA ratio was 111725.1 before vs 1675.3 after eradication, Po0.001) ( Figure 4); this fall in IL-8 is consistent with previous reports. 43,44 The IL-8 mRNA pre-eradication value correlated significantly with histological scores of acute inflammation (R ¼ 0.55, P ¼ 0.004). In contrast, mRNA levels of p27, skp2, and c-myc were not altered significantly by H. pylori eradication.…”

Section: Lcm and Mrna Quantificationmentioning

confidence: 99%

Altered expression of Skp2, c-Myc and p27 proteins but not mRNA after H. pylori eradication in chronic gastritis

et al. 2006

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Helicobacter pylori infection is associated with increased gastric epithelial cell turnover and non-cardia gastric cancer. Cell cycle progression is dependent on the proteasomal degradation of p27, a cyclin-dependent kinase inhibitor and gastric tumor suppressor, following ubiquitination mediated by Skp2. c-Myc is a transcriptional repressor of p27 and also a target of Skp2. In vitro, H. pylori decreases p27 protein post-translationally. We aimed to determine how p27 is regulated by H. pylori in vivo. The effect of eradicating H. pylori on gastric epithelial p27, Skp2, and c-Myc proteins and mRNA was investigated in 22 patients with chronic gastritis, by immunohistochemistry and laser capture microdissection. The percentage of gastric antral epithelial cells expressing p27 protein was significantly higher after eradication of H. pylori (mean7s.e.m. 3772.4% preeradication vs 5572.8% post-eradication; Po0.001), while Skp2 and c-Myc protein-expressing cells were lower (Skp2: 3573.8 vs 2372.6%, P ¼ 0.009; c-Myc: 4773.6 vs 3073.8%, Po0.001). mRNA expressions of p27, Skp2, and c-Myc (normalized for 18SrRNA) were not changed by H. pylori eradication. H. pylori increases c-Myc and decreases gastric epithelial p27 protein expression in association with increased expression of Skp2, the regulator of p27's ubiquitin ligase complex. H. pylori may influence cell cycle progression and carcinogenesis through post-translational effects on specific gene expression.

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“…H. pylori has already been shown to initiate nonspecific immune responses. Infection leads to IL-8 secretion from epithelial cells (17)(18)(19). IL-8 in turn is a potent chemoattractant factor for neutrophils and stimulates the degranulation of these cells (20), thus contributing to the H. pylori-induced tissue damage (21,22).…”

mentioning

confidence: 99%

TheHelicobacter pyloriBlood Group Antigen-Binding Adhesin Facilitates Bacterial Colonization and Augments a Nonspecific Immune Response

Rad¹,

Gerhard²,

Lang

et al. 2002

The Journal of Immunology

160

104

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Presence of the Helicobacter pylori adherence factor blood group Ag-binding adhesin (BabA; binding to Lewisb (Leb)) is associated with ulcer disease, adenocarcinoma, and precancerous lesions. The importance of BabA for bacterial colonization and the inflammatory response is unknown. A total of 141 antral biopsies from H. pylori-infected patients were assessed in regard to the degree of granulocytic (G0°–G3°) and lymphocytic (L1°–L3°) infiltration. DNA genotypes of babA2 (the transcriptionally active gene of BabA), cagA, and vacAs1/2 were determined by PCR. Colonization density and Leb status on gastric epithelial cells were determined by immunohistochemistry. Real-time quantitative (TaqMan) RT-PCR determined mRNA expression of IL-8, TNF -α, and the Th1 markers IFN-γ and the IL-12R β2 chain. A total of 91% of infected patients were Leb positive. The vacAs1+/cagA+ strains harboring babA2 showed significantly higher levels of granulocytic infiltration, bacterial colonization, and IL-8 mRNA than vacAs1+/cagA+ strains lacking babA2. IL-8 mRNA and protein production by KATO III cells in vitro increased dose dependently with addition of different numbers of type 1 strains (G27 and 2808 strains, 0.1–20 bacteria/cell). The mRNA expression of TNF-α, IFN-γ, and IL-12R β2 was higher in H. pylori-positive patients than in controls, but it did not differ significantly between patients infected with different strain types. These data suggest that BabA facilitates colonization of H. pylori and thereby increases IL-8 response, resulting in enhanced mucosal inflammation. Infection with strains harboring BabA thereby augment a nonspecific immune response, whereas the Th1 response toward H. pylori appears to be independent of BabA, cytotoxin-associated gene A, or vacuolating cytotoxin.

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Cytokine gene expression in Helicobacter pylori associated antral gastritis.

Cited by 179 publications

References 20 publications

Possible Association of Atrophic Gastritis and Arterial Stiffness in Healthy Middle-Aged Japanese

Possible Association of Atrophic Gastritis and Arterial Stiffness in Healthy Middle-Aged Japanese

Altered expression of Skp2, c-Myc and p27 proteins but not mRNA after H. pylori eradication in chronic gastritis

TheHelicobacter pyloriBlood Group Antigen-Binding Adhesin Facilitates Bacterial Colonization and Augments a Nonspecific Immune Response

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