Expression of HLA-DR, costimulatory molecules B7-1, B7-2, intercellular adhesion molecule-1 (ICAM-1) and Fas ligand (FasL) on gastric epithelial cells in Helicobacter pylori gastritis; influence of H-pylori eradication

There is evidence that Helicobacter pylori infection up-regulates the expre ssion of HLA class II molecules by gastric epithelial cells (GEC). In this study we evaluated whether GEC are capable of expression of costimulatory m olecules in H. pylori gastritis. The expression of FasL by GEC, before and after eradication of H. pylori, was also studied. Thirty patients (23 men) aged 27-81 years (53.67 +/- 13.99 years (mean +/- s.d.)) with dyspepsia wer e studied. Upper gastrointestinal endoscopy was performed and six biopsies were obtained (antrum, n = 3; corpus, n = 3) for Campylobacter-Like Organis ms (CLO) test and histology; 23 (16 men) were H. pylori(+) and seven (all m en) were H. pylori(-) by both methods and served as controls. Helicobacter pylori eradication therapy was given to H. pylori(+) patients and all patie nts were re-endoscoped after 116 +/- 9 days. Formalin-fixed paraffin-embedd ed tissue sections were stained by the ABC immunoalkaline phosphatase metho d. In H. pylori gastritis HLA-DR was expressed and correlated with disease activity (P < 0.01). No HLA-DR was observed in controls. In H. pylori-eradi cated patients significant decrease of HLA-DR was found (antrum, P < 0.001) . ICAM-1 was expressed by GEC in 80% of H. pylori(+) patients; ICAM-1 expre ssion did not correlate with gastritis parameters and decreased significant ly after eradication (antrum, P < 0.01). B7-1 and B7-2 were expressed on H. pylori(+) samples and their expression decreased after eradication, albeit not significantly. Weak epithelial expression of both B7 molecules was obs erved in all the controls. FasL was steadily expressed by GEC in both H. py lori(+) and H. pylori(-) patients and remained almost unchanged after eradi cation. These findings suggest that GEC may acquire antigen-presenting cell properties in H. pylori infection through de novo expression of HLA-DR and costimulatory molecules. This seems to be attenuated after eradication and resolution of mucosal inflammation. The same cells exhibit the capacity to control the inflammatory process, probably by inducing apoptotic cell deat h to Fas-bearing infiltrating lymphocytes.