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.
journal_name
Gutjournal_title
Gutauthors
Shibata J,Goto H,Arisawa T,Niwa Y,Hayakawa T,Nakayama A,Mori Ndoi
10.1136/gut.45.1.24keywords:
subject
Has Abstractpub_date
1999-07-01 00:00:00pages
24-31issue
1eissn
0017-5749issn
1468-3288journal_volume
45pub_type
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