| Project/Area Number |
09670535
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Nagoya University |
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Principal Investigator |
ARISAWA Tomiyasu School of Medicine, Nagoya University, Assistant, 医学部, 助手 (50273230)
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| Co-Investigator(Kenkyū-buntansha) |
NIWA Yasumasa School of Medicine, Nagoya University, Assistant, 医学部, 助手 (20283442)
GOTO Hidemi School of Medicine, Nagoya University, Assistant, 医学部, 助手 (10215501)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1998: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1997: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | Helicobacter Pylori / Tumor Necrosis Factor / soluble TNF receptor / Apoptosis / Helicobacter Pylori / soluble TNF Receptor / Tumor Necrosis Facter |
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| Research Abstract |
Background & Aims: Tumor Necrosis Factor (TNF) is a predominant cytokine produced in the gastric mucosa of patients with Helicobacter pylori (H.pylori) infection. TNF induces apoptosis in a variety of cells. The soluble TNF receptors (sTNFRs) are divided into sTNF-RI and sTNF-RII, both of which inhibit TNF activity. The aim of this study was to investigate the role of the sTNFRs in H.pylori infection.
Methods: In 40 patients, production of TNF and sTNFRs in the gastric mucosa was measured using biopsy specimens. We examined sTNFRs release in response to TNF and we also examined the protective effect of the sTNFRs against the cytotoxic and apoptotic activity of TNF using gastric epithelial cells.
Results: TNF and sTNFRs expression was significantly higher in H.pylori-positive than H.pylori-negative patients. TNF dose-dependently induced sTNF-RI release from gastric epithelial cells. sTNF-RII was also released from the cells. TNF decreased cell viability, but the effect was very weak. A combination of anti-sTNF-RI and sTNF-RII monoclonal antibodies significantly increased TNF induced cytotoxicity and apoptosis of gastric epithelial cells.
Conclusions: The sTNFRs appear to protect gastric epithelial cells from TNF induced apoptosis in H.pylori infection.
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