Free radicals in helicobacter pylori infection

Hidekazu Suzuki, Toshihiro Nishizawa, Hitoshi Tsugawa, Toshifumi Hibi

研究成果: Chapter

1 引用 (Scopus)

抄録

Helicobacter pylori infection, which is the main cause of gastritis, peptic ulcer disease and gastric cancer, is associated with infiltration of the gastric mucosa by neutrophils, macrophages, and B and T lymphocytes. However, this immune and inflammatory response cannot completely control the bacterial infection, and leaves the host prone to complications resulting from persistent inflammation. As a result, H. pylori infection may cause chronic inflammation, accumulation of reactive oxygen species, and oxidative DNA damage in the gastric mucosa. The H. pylori bacterial effector proteins are transported into the gastric host cells via the type IV secretory system, and regulate intracellular signal transduction. This mechanism provides novel insight into how H. pylori survives in the acidic environment of the human stomach. In cases with persistent gastric infection, the chronic gastritis may remain asymptomatic or may evolve into more severe diseases, such as peptic ulcer disease and chronic atrophic gastritis. In addition, infection with H. pylori increases the risk of development of gastric cancer and mucosa-associated lymphoid tissue lymphoma. This review focuses on the oxidative mechanisms involved in the bacterial and host-mucosal responses during colonization of the gastric mucosa by H. pylori.

元の言語English
ホスト出版物のタイトルFrontiers of Gastrointestinal Research
ページ111-120
ページ数10
29
DOI
出版物ステータスPublished - 2010 12

出版物シリーズ

名前Frontiers of Gastrointestinal Research
29
ISSN(印刷物)03020665

Fingerprint

Helicobacter Infections
Helicobacter pylori
Free Radicals
Gastric Mucosa
Stomach
Gastritis
Peptic Ulcer
Stomach Neoplasms
Inflammation
Atrophic Gastritis
Marginal Zone B-Cell Lymphoma
Bacterial Proteins
Infection
Bacterial Infections
DNA Damage
Reactive Oxygen Species
Signal Transduction
Neutrophils
B-Lymphocytes
Chronic Disease

ASJC Scopus subject areas

  • Gastroenterology

これを引用

Suzuki, H., Nishizawa, T., Tsugawa, H., & Hibi, T. (2010). Free radicals in helicobacter pylori infection. : Frontiers of Gastrointestinal Research (巻 29, pp. 111-120). (Frontiers of Gastrointestinal Research; 巻数 29). https://doi.org/10.1159/00031997910

Free radicals in helicobacter pylori infection. / Suzuki, Hidekazu; Nishizawa, Toshihiro; Tsugawa, Hitoshi; Hibi, Toshifumi.

Frontiers of Gastrointestinal Research. 巻 29 2010. p. 111-120 (Frontiers of Gastrointestinal Research; 巻 29).

研究成果: Chapter

Suzuki, H, Nishizawa, T, Tsugawa, H & Hibi, T 2010, Free radicals in helicobacter pylori infection. : Frontiers of Gastrointestinal Research. 巻. 29, Frontiers of Gastrointestinal Research, 巻. 29, pp. 111-120. https://doi.org/10.1159/00031997910
Suzuki H, Nishizawa T, Tsugawa H, Hibi T. Free radicals in helicobacter pylori infection. : Frontiers of Gastrointestinal Research. 巻 29. 2010. p. 111-120. (Frontiers of Gastrointestinal Research). https://doi.org/10.1159/00031997910
Suzuki, Hidekazu ; Nishizawa, Toshihiro ; Tsugawa, Hitoshi ; Hibi, Toshifumi. / Free radicals in helicobacter pylori infection. Frontiers of Gastrointestinal Research. 巻 29 2010. pp. 111-120 (Frontiers of Gastrointestinal Research).
@inbook{b72968f0917f420ab7df2fc4e9226fd1,
title = "Free radicals in helicobacter pylori infection",
abstract = "Helicobacter pylori infection, which is the main cause of gastritis, peptic ulcer disease and gastric cancer, is associated with infiltration of the gastric mucosa by neutrophils, macrophages, and B and T lymphocytes. However, this immune and inflammatory response cannot completely control the bacterial infection, and leaves the host prone to complications resulting from persistent inflammation. As a result, H. pylori infection may cause chronic inflammation, accumulation of reactive oxygen species, and oxidative DNA damage in the gastric mucosa. The H. pylori bacterial effector proteins are transported into the gastric host cells via the type IV secretory system, and regulate intracellular signal transduction. This mechanism provides novel insight into how H. pylori survives in the acidic environment of the human stomach. In cases with persistent gastric infection, the chronic gastritis may remain asymptomatic or may evolve into more severe diseases, such as peptic ulcer disease and chronic atrophic gastritis. In addition, infection with H. pylori increases the risk of development of gastric cancer and mucosa-associated lymphoid tissue lymphoma. This review focuses on the oxidative mechanisms involved in the bacterial and host-mucosal responses during colonization of the gastric mucosa by H. pylori.",
author = "Hidekazu Suzuki and Toshihiro Nishizawa and Hitoshi Tsugawa and Toshifumi Hibi",
year = "2010",
month = "12",
doi = "10.1159/00031997910",
language = "English",
isbn = "9783805596091",
volume = "29",
series = "Frontiers of Gastrointestinal Research",
pages = "111--120",
booktitle = "Frontiers of Gastrointestinal Research",

}

TY - CHAP

T1 - Free radicals in helicobacter pylori infection

AU - Suzuki, Hidekazu

AU - Nishizawa, Toshihiro

AU - Tsugawa, Hitoshi

AU - Hibi, Toshifumi

PY - 2010/12

Y1 - 2010/12

N2 - Helicobacter pylori infection, which is the main cause of gastritis, peptic ulcer disease and gastric cancer, is associated with infiltration of the gastric mucosa by neutrophils, macrophages, and B and T lymphocytes. However, this immune and inflammatory response cannot completely control the bacterial infection, and leaves the host prone to complications resulting from persistent inflammation. As a result, H. pylori infection may cause chronic inflammation, accumulation of reactive oxygen species, and oxidative DNA damage in the gastric mucosa. The H. pylori bacterial effector proteins are transported into the gastric host cells via the type IV secretory system, and regulate intracellular signal transduction. This mechanism provides novel insight into how H. pylori survives in the acidic environment of the human stomach. In cases with persistent gastric infection, the chronic gastritis may remain asymptomatic or may evolve into more severe diseases, such as peptic ulcer disease and chronic atrophic gastritis. In addition, infection with H. pylori increases the risk of development of gastric cancer and mucosa-associated lymphoid tissue lymphoma. This review focuses on the oxidative mechanisms involved in the bacterial and host-mucosal responses during colonization of the gastric mucosa by H. pylori.

AB - Helicobacter pylori infection, which is the main cause of gastritis, peptic ulcer disease and gastric cancer, is associated with infiltration of the gastric mucosa by neutrophils, macrophages, and B and T lymphocytes. However, this immune and inflammatory response cannot completely control the bacterial infection, and leaves the host prone to complications resulting from persistent inflammation. As a result, H. pylori infection may cause chronic inflammation, accumulation of reactive oxygen species, and oxidative DNA damage in the gastric mucosa. The H. pylori bacterial effector proteins are transported into the gastric host cells via the type IV secretory system, and regulate intracellular signal transduction. This mechanism provides novel insight into how H. pylori survives in the acidic environment of the human stomach. In cases with persistent gastric infection, the chronic gastritis may remain asymptomatic or may evolve into more severe diseases, such as peptic ulcer disease and chronic atrophic gastritis. In addition, infection with H. pylori increases the risk of development of gastric cancer and mucosa-associated lymphoid tissue lymphoma. This review focuses on the oxidative mechanisms involved in the bacterial and host-mucosal responses during colonization of the gastric mucosa by H. pylori.

UR - http://www.scopus.com/inward/record.url?scp=78751547529&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=78751547529&partnerID=8YFLogxK

U2 - 10.1159/00031997910

DO - 10.1159/00031997910

M3 - Chapter

AN - SCOPUS:78751547529

SN - 9783805596091

VL - 29

T3 - Frontiers of Gastrointestinal Research

SP - 111

EP - 120

BT - Frontiers of Gastrointestinal Research

ER -