Regulation of tumour necrosis factor (TNF) induced apoptosis by soluble TNF receptors in Helicobacter pyloriinfection. Issue 1 (1st July 1999)

• Record Type: Journal Article
• Authors: Shibata, J; Goto, H; Arisawa, T; Niwa, Y; Hayakawa, T; Nakayama, A; Mori, N
• Is Part Of: Gut. Volume 45:Issue 1(1999)
• Page Start: 24
• Page End: 31
• Publication Date: 1999-07-01
• Subjects: Helicobacter pylori -- tumour necrosis factor -- soluble TNF receptors -- apoptosis -- gastric mucosa -- stomach; Gastroenterology -- Periodicals; 616.33
• DOI: 10.1136/gut.45.1.24
• Languages: English
• ISSNs: 0017-5749

Abstract

Abstract : BACKGROUND: Tumour necrosis factor (TNF) is a predominant cytokine produced in the gastric mucosa of patients with Helicobacter pylori infection. TNF induces apoptosis in a variety of cells. The soluble TNF receptors (sTNF-Rs) can be divided into sTNF-RI and sTNF-RII, both of which inhibit TNF activity. However, their precise mechanisms remain unclear. AIM: To investigate the role of sTNF-Rs in H pylori infection. METHODS: In 40 patients, production of TNF and sTNF-Rs in gastric mucosa was measured using biopsy specimens. In addition, in gastric epithelial cells, sTNF-R release in response to TNF and the protective effect of sTNF-Rs against the cytotoxic and apoptotic activities of TNF were examined. RESULTS: TNF and sTNF-R 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 small. A combination of anti-sTNF-RI and anti-sTNF-RII monoclonal antibodies significantly increased TNF induced cytotoxicity and apoptosis of gastric epithelial cells. CONCLUSIONS: These results show that sTNF-Rs are actively produced in H pylori infected gastric mucosa. sTNF-Rs appear to protect gastric epithelial cells from TNF induced apoptosis in H pylori infection.