Free radicals in Helicobacter pylori infection

Hidekazu Suzuki, Toshihiro Nishizawa, Hitoshi Tsugawa, Toshifumi Hibi

Research output: Chapter in Book/Report/Conference proceedingChapter

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.

Original languageEnglish
Title of host publicationFree Radical Biology in Digestive Diseases
PublisherS. Karger AG
Pages111-120
Number of pages10
Volume29
ISBN (Print)9783805596107, 9783805596091
DOIs
Publication statusPublished - 2010 Dec 21

Fingerprint

Helicobacter Infections
infectious diseases
Helicobacter pylori
free radicals
Free Radicals
Gastric Mucosa
ulcers
Stomach
Gastritis
Peptic Ulcer
Signal transduction
cancer
Stomach Neoplasms
T-cells
Macrophages
neutrophils
effectors
stomach
Infiltration
macrophages

ASJC Scopus subject areas

  • Medicine(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Physics and Astronomy(all)

Cite this

Suzuki, H., Nishizawa, T., Tsugawa, H., & Hibi, T. (2010). Free radicals in Helicobacter pylori infection. In Free Radical Biology in Digestive Diseases (Vol. 29, pp. 111-120). S. Karger AG. https://doi.org/10.1159/000319979

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

Free Radical Biology in Digestive Diseases. Vol. 29 S. Karger AG, 2010. p. 111-120.

Research output: Chapter in Book/Report/Conference proceedingChapter

Suzuki, H, Nishizawa, T, Tsugawa, H & Hibi, T 2010, Free radicals in Helicobacter pylori infection. in Free Radical Biology in Digestive Diseases. vol. 29, S. Karger AG, pp. 111-120. https://doi.org/10.1159/000319979
Suzuki H, Nishizawa T, Tsugawa H, Hibi T. Free radicals in Helicobacter pylori infection. In Free Radical Biology in Digestive Diseases. Vol. 29. S. Karger AG. 2010. p. 111-120 https://doi.org/10.1159/000319979
Suzuki, Hidekazu ; Nishizawa, Toshihiro ; Tsugawa, Hitoshi ; Hibi, Toshifumi. / Free radicals in Helicobacter pylori infection. Free Radical Biology in Digestive Diseases. Vol. 29 S. Karger AG, 2010. pp. 111-120
@inbook{64ac25894616418a96590ea3d24544bd,
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",
day = "21",
doi = "10.1159/000319979",
language = "English",
isbn = "9783805596107",
volume = "29",
pages = "111--120",
booktitle = "Free Radical Biology in Digestive Diseases",
publisher = "S. Karger AG",

}

TY - CHAP

T1 - Free radicals in Helicobacter pylori infection

AU - Suzuki, Hidekazu

AU - Nishizawa, Toshihiro

AU - Tsugawa, Hitoshi

AU - Hibi, Toshifumi

PY - 2010/12/21

Y1 - 2010/12/21

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=84925859478&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84925859478&partnerID=8YFLogxK

U2 - 10.1159/000319979

DO - 10.1159/000319979

M3 - Chapter

SN - 9783805596107

SN - 9783805596091

VL - 29

SP - 111

EP - 120

BT - Free Radical Biology in Digestive Diseases

PB - S. Karger AG

ER -