ID | 118920 |
Author |
Ojima, Hinako
Okayama University
Kuraoka, Sakiko
Okayama University
Okanoue, Shyoutarou
Okayama University
Okada, Hiroyuki
Himeji Red Cross Hospital
Gotoh, Kazuyoshi
Okayama University
Matsushita, Osamu
Okayama University
Watanabe, Akari
Tokushima University
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Yokota, Kenji
Okayama University
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Keywords | Helicobacter pylori
nitrate-reducing bacteria
IL-8
TNF-α
cell cycle
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Content Type |
Journal Article
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Description | Helicobacter pylori infection is an important risk factor for developing gastric cancer. However, only a few H. pylori-infected people develop gastric cancer. Thus, other risk factors aside from H. pylori infection may be involved in gastric cancer development. This study aimed to investigate whether the nitrate-reducing bacteria isolated from patients with atrophic gastritis caused by H. pylori infection are risk factors for developing atrophic gastritis and gastric neoplasia. Nitrate-reducing bacteria were isolated from patients with atrophic gastritis caused by H. pylori infection. Among the isolated bacteria, Actinomyces oris, Actinomyces odontolyticus, Rothia dentocariosa, and Rothia mucilaginosa were used in the subsequent experiments. Cytokine inducibility was evaluated in monocytic cells, and mitogen-activated protein kinase (MAPK) activity and cell cycle were assessed in the gastric epithelial cells. The cytotoxicities and neutrophil-inducing abilities of the Actinomyces and Rothia species were enhanced when cocultured with H. pylori. Th1/Th2-related cytokines were also expressed, but their expression levels differed depending on the bacterial species. Moreover, H. pylori and Actinomyces activated MAPK (ERK and p38) and affected cell cycle progression. Some nitrate-reducing bacteria cocultured with H. pylori may promote inflammation and atrophy by inducing cytokine production. In addition, the MAPK activation and cell cycle progression caused by these bacteria can contribute to gastric cancer development.
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Journal Title |
Microorganisms
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ISSN | 20762607
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Publisher | MDPI
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Volume | 10
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Issue | 12
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Start Page | 2495
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Published Date | 2022-12-16
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Rights | This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
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EDB ID | |
DOI (Published Version) | |
URL ( Publisher's Version ) | |
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language |
eng
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TextVersion |
Publisher
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departments |
Oral Sciences
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