Induction of gastric epithelial apoptosis by Helicobacter pylori.

Moss, Steven F.; Calam, J.; Agarwal, Banke; Wang, S; Holt, Peter R.

doi:10.1136/gut.38.4.498

Cited by 380 publications

(273 citation statements)

References 15 publications

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“…Notably, our present study demonstrates that survivin expression correlates with the severity of gastritis and H. pylori infection in non-cancer patients. On the other hand, this appears to contradict with the observation that chronic gastritis and H. pylori infection is associated with increased epithelial cell apoptosis (Attallah et al, 1996;Moss et al, 1996;Wagner et al, 1997;Leung et al, 2000b). We speculated that the increased survivin expression in these tissues may be secondary to the pro-apoptotic stimuli induced by H. pylori.…”

Section: Discussionmentioning

confidence: 56%

Increased expression of survivin in gastric cancer patients and in first degree relatives

Leung

Ebert

et al. 2002

Br J Cancer

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Survivin was recently described as an apoptosis inhibitor. Its pathogenic role in gastric cancer is largely unknown. Expression of survivin in gastric cancer and non-cancer first-degree relatives, and its association with apoptosis and cyclo-oxygenase-2 expression was investigated. Fifty gastric cancer, 30 non-cancer first-degree relatives, 20 normal controls and five gastric cancer cell lines were studied. Survivin and cyclo-oxygenase-2 were evaluated by reverse transcriptase-polymerase chain reaction, immunohistochemistry and Western blot. Survivin expression was absent from normal gastric mucosa. All five cancer cell lines and 34 out of 50 (68%) human gastric cancer tissues expressed survivin mRNA. Survivin expression was less frequent (22%; P50.001) in adjacent non-tumour gastric tissues. Immunohistochemistry and Western blot obtained similar findings. Gastric cancers with survivin expression displayed significantly reduced apoptosis (P=0.02), and associated with cyclo-oxygenase-2 overexpression at both mRNA (P=0.001) and protein levels (P=0.041). Moreover, survivin mRNA was detected in the gastric mucosa of eight (27%) non-cancer relatives. Expression in non-cancer patients showed positive correlation with H. pylori infection (P=0.004). This demonstrates the frequent expression of survivin in gastric cancer and in first-degree relatives. Coexpression of survivin and cyclo-oxygenase-2 may suggest multiple pathways contributing to the inhibition of apoptosis in gastric cancer.

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Section: Discussionmentioning

confidence: 56%

Increased expression of survivin in gastric cancer patients and in first degree relatives

Leung

Ebert

et al. 2002

Br J Cancer

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“…Attachment of the bacteria to the epithelial cells also induces actin polymerization and the phosphorylation of cellular proteins (7,8), which may be reflective of the stimulation of signaling mechanisms that lead to programmed cell death. Apoptosis of the gastric epithelium has been reported to be increased in the infected mucosa (10,30) and may be a mechanism for the epithelial damage that leads to ulcer formation or atrophy. Because H. pylori is not an invasive bacterium, the injury associated with the attachment of H. pylori to the gastric epithelium must be due to the interactions between bacterial and host cell surface proteins that are capable of delivering intracellular signals.…”

Section: Discussionmentioning

confidence: 99%

“…One of the consequences of the signals initiated during H. pylori adhesion to cultured gastric epithelial cells is increased apoptosis of the epithelium, which has been noted to occur in vivo (9,10). Thus, the bacterial structures responsible for adhesion and stimulation of host cell death may be regarded as important virulence factors.…”

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confidence: 99%

Helicobacter pylori Urease Binds to Class II MHC on Gastric Epithelial Cells and Induces Their Apoptosis

Fan

Gunasena

Cheng

et al. 2000

The Journal of Immunology

146

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Infection by Helicobacter pylori leads to injury of the gastric epithelium and a cellular infiltrate that includes CD4+ T cells. H. pylori binds to class II MHC molecules on gastric epithelial cells and induces their apoptosis. Because urease is an abundant protein expressed by H. pylori, we examined whether it had the ability to bind class II MHC and induce apoptosis in class II MHC-bearing cells. Flow cytometry revealed the binding of PE-conjugated urease to class II MHC+ gastric epithelial cell lines. The binding of urease to human gastric epithelial cells was reduced by anti-class II MHC Abs and by staphylococcal enterotoxin B. The binding of urease to class II MHC was confirmed when urease bound to HLA-DR1-transfected COS-1 (1D12) cells but not to untransfected COS-1 cells. Urease also bound to a panel of B cell lines expressing various class II MHC alleles. Recombinant urease induced apoptosis in gastric epithelial cells that express class II MHC molecules, but not in class II MHC− cells. Also, Fab from anti-class II MHC and not from isotype control Abs blocked the induction of apoptosis by urease in a concentration-dependent manner. The adhesin properties of urease might point to a novel and important role of H. pylori urease in the pathogenesis of H. pylori infection.

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“…However; this balance can be affected by H. pylori infection. H. pylori infection has been reported to be associated with increased (Mannick et al, 1996;Moss et al, 1996;Moss, 1998;Peek et al, 1999), unaltered (Peek et al, 1997) and decreased (Zhong et al, 2001) levels of apoptosis in gastric mucosa. P53 is a tumor suppressor gene, located on chromosome 17p13.…”

Section: Introductionmentioning

confidence: 99%

Helicobacter pylori Infection and a P53 Codon 72 Single Nucleotide Polymorphism: a Reason for an Unexplained Asian Enigma

Pandey¹,

Misra²,

Misra³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Aim: P53, the most commonly mutated tumor suppressor gene in all types of human cancer, is involved in cell cycle arrest and control of apoptosis. Although p53 contains several polymorphic sites, the codon 72 polymorphism is by far more common. There are divergent reports but many studies suggest p53 pro/pro SNP may be associated with susceptibility to developing various cancers in different regions of the world. The present study aimed to find any correlation between H. pylori infection and progression of carcinogenesis, by studying apoptosis and the p53 gene in gastric biopsies from north Indian population. Materials and Methods: A total of 921 biopsies were collected and tested for prevalence of H. pylori by rapid urease test (RUT), imprint cytology and histology. Apoptosis was studied by the TUNEL method. Analysis of p53 gene polymorphism at codon 72 was accomplished by PCR using restriction enzyme BstU1. Observation: Out of 921 samples tested 56.7% (543) were H. pylori positive by the three techniques. The mean apoptotic index (AI) in the normal group was 2.12, while gastritis had the maximum 4.24 followed by gastric ulcer 2.28, gastropathy 2.22 and duodenal ulcer 2.08. Mean AI in cases with gastric cancer (1.72) was less than the normal group. The analysis of p53 72 SNP revealed that p53 (Arg/Arg), (Pro /Arg) variant are higher (40.59% & 33.66%) as compared to p53 pro/pro variant (25.74%) inthe healthy population. Conclusions: The North Indian population harbors Arg or Pro/Arg SNP that is capable of withstanding stress conditions; this may be the reason of low incidence of gastric disease in spite of high infection with H. pylori. There was no significant association with H. pylori infection and AI. However, there is increased apoptosis in gastritis which may occur independent of H. pylori or p53 polymorphism.

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Induction of gastric epithelial apoptosis by Helicobacter pylori.

Cited by 380 publications

References 15 publications

Increased expression of survivin in gastric cancer patients and in first degree relatives

Increased expression of survivin in gastric cancer patients and in first degree relatives

Helicobacter pylori Urease Binds to Class II MHC on Gastric Epithelial Cells and Induces Their Apoptosis

Helicobacter pylori Infection and a P53 Codon 72 Single Nucleotide Polymorphism: a Reason for an Unexplained Asian Enigma

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