Helicobacter pylori and acetylsalicylic acid synergistically accelerate apoptosis via Fas antigen pathway in rabbit gastric epithelial cells

The mechanism for gastric epithelial cellular apoptosis by both H. pylori and NSAIDs remains unknown. Normal gastric epithelial cells, collected from rabbit stomach, were cultured with viable H. pylori and/or an acetylsalicylic acid for 24 hr as an in vitro model of gastric epithelial cell injury. T...

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Bibliographic Details
Published in:Digestive diseases and sciences 2002-04, Vol.47 (4), p.809-817
Main Authors: WATANABE, Kazuhiro, HOSHIYA, Satoshi, TOKUNAGA, Kengo, TANAKA, Akifumi, WATANABE, Hidehiro, NAGAMATSU, Shinya, ISHIDA, Hitoshi, TAKAHASHI, Shin'Ichi
Format: Article
Language:English
Subjects:
Animals
Anti-Inflammatory Agents, Non-Steroidal - pharmacology
Antigens, Bacterial
Apoptosis - drug effects
Aspirin - pharmacology
Bacterial diseases
Bacterial diseases of the digestive system and abdomen
Bacterial Proteins - genetics
Biological and medical sciences
Cell Line
DNA Fragmentation
fas Receptor - physiology
Gastric Mucosa - cytology
Gastric Mucosa - drug effects
Gastric Mucosa - microbiology
Gastric Mucosa - physiopathology
Helicobacter Infections - physiopathology
Helicobacter pylori - genetics
Human bacterial diseases
Immunoblotting
Infectious diseases
L-Lactate Dehydrogenase - metabolism
Medical sciences
Rabbits
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Summary:The mechanism for gastric epithelial cellular apoptosis by both H. pylori and NSAIDs remains unknown. Normal gastric epithelial cells, collected from rabbit stomach, were cultured with viable H. pylori and/or an acetylsalicylic acid for 24 hr as an in vitro model of gastric epithelial cell injury. The Fas antigen expression rate in the gastric epithelial cells was measured using a FACScan. In group E, in which H. pylori inoculation of epithelial cells was followed by treatment with an NSAID, the rate of Fas antigen expression was significantly higher than the rate observed after treatment with either H. pylori or NSAID alone. Despite the fact that drug treatment alone did not significantly increase the Fas expression rate vs control cells. The results suggest that H. pylori and NSAID induce gastric cell injury as apoptosis via the Fas antigen pathway in a synergistic manner and that this effect is particularly strong when NSAID treatment follows H. pylori infection.
ISSN:0163-2116
1573-2568
DOI:10.1023/A:1014752303138