ID 83815
Author
Kawahara, Tsukasa Department of Nutritional Physiology, The University of Tokushima School of Medicine
Kuwano, Yuki Department of Nutritional Physiology, The University of Tokushima School of Medicine Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Teshima-Kondo, Shigetada Department of Nutritional Physiology, The University of Tokushima School of Medicine KAKEN Search Researchers
Sugiyama, Toshiro Third Department of Internal Medicine, Hokkaido University School of Medicine
Kawai, Tomoko Department of Nutritional Physiology, The University of Tokushima School of Medicine
Nikawa, Takeshi Department of Nutritional Physiology, The University of Tokushima School of Medicine Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Kishi, Kyoichi Department of Nutritional Physiology, The University of Tokushima School of Medicine Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Rokutan, Kazuhito Department of Nutritional Physiology, The University of Tokushima School of Medicine Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Keywords
apoptosis
Helicobacter pylori
cag PAI gene
LPS
gastric mucosal cells
Content Type
Journal Article
Description
The cag pathogenicity island (cag PAI) genes are a major determinant of virulence of Helicobacter pylori (Hp). Lipopolysaccharide (LPS) purified from the cag PAI-positive (type I) strains induced apoptosis of primary cultures of guinea pig gastric mucosal cells. Lipid A catalyzed this apoptosis. These cells expressed the Toll-like receptor 4 (TLR4) mRNA and its protein, and type I Hp LPS phosphorylated transforming growth factor β-activated kinase 1 (TAK1) and TAK1-binding protein 1 (TAB1) in association with up-regulation of the TLR4 expressions, suggesting that type I Hp LPS evoked distinct TLR4 signaling. In contrast, Hp LPS from type II strains with complete or partial deletion of the cag PAI genes did not phosphorylate TAK1 and TAB1 and failed to induce apoptosis. Accelerated apoptosis of gastric epithelial cells is one of the important events relevant to chronic, atrophic gastritis caused by Hp infection. The difference in proapoptotic action of LPS between the type I and II strains may support an important role of the cag PAI genes in the pathogenesis of gastric lesions caused by Hp infection.
Journal Title
The journal of medical investigation : JMI
ISSN
13431420
NCID
AA11166929
Volume
48
Issue
3-4
Start Page
166
End Page
174
Sort Key
166
Published Date
2001
Remark
EDB ID
FullText File
language
eng
departments
Medical Sciences