[Regulation of Fas expression in gastric epithelium: one of the auto-immune mechanisms of Helicobacter pylori pathogenesis].
OBJECTIVE
To investigate the pathogenic mechanism of Helicobacter pylori (H.pylori)-mediated gastric epithelial cell damage.


METHODS
Fas expressions in gastric epithelial cell lines and freshly isolated gastric epithelial cells with or without H.pylori infection were evaluated by flow cytometry. The modulation of Fas expression in gastric epithelial cells by H.pylori or by Th1 cytokines present in H.pylori-infected gastric mucosa was assessed in vitro. The function of Fas expressed by the gastric epithelial cells to induce cell apoptosis was determined by enzyme-linked immunosorbent assay (ELISA) after incubation of the cells with anti-Fas antibody.


RESULTS
All of the three gastric epithelial cell lines, AGS, N87 and kato-III, expressed detectable Fas protein when examined by flow cytometry. The percentage of positive cells and the amount of Fas protein on cell surface were larger in freshly isolated gastric epithelial cells with H.pylori infection than in uninfected cells (P<0.05). H. pylori alone or in combination with Th1 cytokines (IFN-gamma and TNF-alpha) significantly increased the expression of Fas in gastric epithelial cell lines in vitro. After incubation with IgM anti-Fas mAb, Fas-bearing gastric epithelial cells underwent apoptosis, and this effect of Fas was enhanced by IFN-gamma.


CONCLUSIONS
Th1 cells accumulated in the gastric mucosa during H.pylori infection is involved in the damage of gastric epithelium through the modulation of Fas/Fas ligand interaction.
Wang
Ji-de
JD
Institute for Digestive Diseases of PLA, Nanfang Hospital, First Military Medical University, Guangzhou 510515, China. jdwang88@hotmail.com
Bai
Yang
Y
Lin
Huan-jian
HJ
Zhang
Ya-li
YL
Huang
Wen
W
Zhou
Dian-yuan
DY
D017209:Apoptosis; D015551:Autoimmunity; D005753:Gastric Mucosa / Q000737:chemistry* / Q000473:pathology; D016481:Helicobacter Infections / Q000209:etiology* / Q000276:immunology; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006801:Humans; D007371:Interferon-gamma / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D019014:fas Receptor / Q000032:analysis*
D014409:Tumor Necrosis Factor-alpha; D019014:fas Receptor; D007371:Interferon-gamma