Helicobacter pylori Infection Introduces DNA Double-Strand Breaks in Host Cells

Hanada, Katsuhiro; Uchida, Tomohisa; Tsukamoto, Yoshiyuki; Watada, Masahide; Yamaguchi, Nahomi; Yamamoto, Kaoru; Shiota, Seiji; Moriyama, Masatsugu; Graham, David Y.; Yamaoka, Yoshio

doi:10.1128/iai.02368-14

Cited by 93 publications

(95 citation statements)

References 26 publications

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“…H pylori -induced inflammation leads to high gastric endothelial cell turnover and a microenvironment that is high in reactive oxygen and nitrogen species, increasing opportunities for DNA damage and somatic mutations 3, 27-29 (Figure 2). H pylori can induce methylation of multiple CpG islands, especially at sites encoding tumor suppressors such as E-cadherin 30 .…”

Section: H Pylori-associated Gastric Cancermentioning

confidence: 99%

Helicobacter pylori Update: Gastric Cancer, Reliable Therapy, and Possible Benefits

2015

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Helicobacter pylori infection contributes to development of diverse gastric and extra-gastric diseases. The infection is necessary but not sufficient for development of gastric adenocarcinoma. Its eradication would eliminate a major worldwide cause of cancer death, so there is much interest in identifying how, if, and when this can be accomplished. There are several mechanisms by which H pylori contributes to development of gastric cancer. Gastric adenocarcinoma is one of many cancers associated with inflammation, which is induced by H pylori infection, yet the bacteria also cause genetic and epigenetic changes that lead to genetic instability in gastric epithelial cells. H pylori eradication reduces both. However, many factors must be considered in determining whether treating this bacterial infection will prevent cancer or only reduce its risk—these must be considered in designing reliable and effective eradication therapies. Furthermore, H pylori infection has been proposed to provide some benefits, such as reducing the risks of obesity or childhood asthma, although there are no convincing data to support the benefits of H pylori infections.

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Section: H Pylori-associated Gastric Cancermentioning

confidence: 99%

Helicobacter pylori Update: Gastric Cancer, Reliable Therapy, and Possible Benefits

2015

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“…The presence of cagA in a strain results in an increased risk of gastric carcinogenesis compared with individuals infected with CagA-negative strains 26 . Increased hydrogen peroxide levels and oxidative DNA damage are seen with CagA-positive strains 27, 28. In addition, there is an increase in tumor necrosis factor-α and IL8, which are inflammatory and oxidative stress markers 29 .…”

Section: Oxidative Stress Generationmentioning

confidence: 99%

Oxidative Stress Resulting From Helicobacter pylori Infection Contributes to Gastric Carcinogenesis

Butcher

Hartog

Ernst

et al. 2017

Cellular and Molecular Gastroenterology and Hepatology

184

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Helicobacter pylori is a gram-negative, microaerophilic bacterium that infects the stomach and can lead to, among other disorders, the development of gastric cancer. The inability of the host to clear the infection results in a chronic inflammatory state with continued oxidative stress within the tissue. Reactive oxygen species and reactive nitrogen species produced by the immune and epithelial cells damage the host cells and can result in DNA damage. H pylori has evolved to evoke this damaging response while blunting the host’s efforts to kill the bacteria. This long-lasting state with inflammation and oxidative stress can result in gastric carcinogenesis. Continued efforts to better understand the bacterium and the host response will serve to prevent or provide improved early diagnosis and treatment of gastric cancer.

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“…; Hanada et al . ). To detect infection‐induced DSBs, it is important to distinguish between DNA of host and microbial origin.…”

Section: Resultsmentioning

confidence: 97%

Detection of DNA double‐strand breaks by pulsed‐field gel electrophoresis

et al. 2016

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A DNA double-strand break (DSB) is one of the most cytotoxic DNA lesions because unrepaired DSBs cause chromosomal aberrations and cell death. Although many physiological DSBs occur at DNA replication sites, the molecular mechanisms underlying this remain poorly understood. There was therefore a need to develop a highly specific method to detect DSB fragments containing DNA replication sites. Here we investigated whether pulsed-field gel electrophoresis (PFGE) combined with visualization of DNA replication sites by immunoblotting using halogenized deoxyuridines, such as BrdU and IdU, was sufficient for this detection. Our methodology enabled us to reproduce previously reported data. In addition, this methodology was also applied to the detection of bacterial infection-induced DSBs on human chromosomal DNA. Based on our findings, we propose that this strategy combining PFGE with immunoblot analysis will be applicable to studies analyzing the mechanistic details of DNA repair, the DNA damage response and the activity of DNA-damaging agents.

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Helicobacter pylori Infection Introduces DNA Double-Strand Breaks in Host Cells

Cited by 93 publications

References 26 publications

Helicobacter pylori Update: Gastric Cancer, Reliable Therapy, and Possible Benefits

Helicobacter pylori Update: Gastric Cancer, Reliable Therapy, and Possible Benefits

Oxidative Stress Resulting From Helicobacter pylori Infection Contributes to Gastric Carcinogenesis

Detection of DNA double‐strand breaks by pulsed‐field gel electrophoresis

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