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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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| Published in: | Digestive diseases and sciences 2002-04, Vol.47 (4), p.809-817 |
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| Main Authors: | , , , , , , , |
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| container_end_page | 817 |
| container_issue | 4 |
| container_start_page | 809 |
| container_title | Digestive diseases and sciences |
| container_volume | 47 |
| creator | WATANABE, Kazuhiro HOSHIYA, Satoshi TOKUNAGA, Kengo TANAKA, Akifumi WATANABE, Hidehiro NAGAMATSU, Shinya ISHIDA, Hitoshi TAKAHASHI, Shin'Ichi |
| description | 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. |
| doi_str_mv | 10.1023/A:1014752303138 |
| format | article |
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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.</description><identifier>ISSN: 0163-2116</identifier><identifier>EISSN: 1573-2568</identifier><identifier>DOI: 10.1023/A:1014752303138</identifier><identifier>PMID: 11991615</identifier><identifier>CODEN: DDSCDJ</identifier><language>eng</language><publisher>Heidelberg: Springer</publisher><subject>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</subject><ispartof>Digestive diseases and sciences, 2002-04, Vol.47 (4), p.809-817</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright Kluwer Academic Publishers Apr 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13655151$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11991615$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>WATANABE, Kazuhiro</creatorcontrib><creatorcontrib>HOSHIYA, Satoshi</creatorcontrib><creatorcontrib>TOKUNAGA, Kengo</creatorcontrib><creatorcontrib>TANAKA, Akifumi</creatorcontrib><creatorcontrib>WATANABE, Hidehiro</creatorcontrib><creatorcontrib>NAGAMATSU, Shinya</creatorcontrib><creatorcontrib>ISHIDA, Hitoshi</creatorcontrib><creatorcontrib>TAKAHASHI, Shin'Ichi</creatorcontrib><title>Helicobacter pylori and acetylsalicylic acid synergistically accelerate apoptosis via Fas antigen pathway in rabbit gastric epithelial cells</title><title>Digestive diseases and sciences</title><addtitle>Dig Dis Sci</addtitle><description>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. 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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.</abstract><cop>Heidelberg</cop><pub>Springer</pub><pmid>11991615</pmid><doi>10.1023/A:1014752303138</doi><tpages>9</tpages></addata></record> |
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| 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 |
| title | Helicobacter pylori and acetylsalicylic acid synergistically accelerate apoptosis via Fas antigen pathway in rabbit gastric epithelial cells |
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