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Abstract

Chronic atrophic gastritis can be induced either by H. pylori or by an autoimmune process. The protein product of bcl-2, which is a protooncogene, blocks apoptosis. Aberrant bcl-2 expression has been found in 68% of atrophic gastritis patients. The aim of this study was to compare bcl-2 expression in 20 autoimmune atrophic gastritis patients to that in 20 H. pylori-associated atrophic gastritis patients. Twenty patients with H. pylori antral gastritis but without atrophy served as controls. The bcl-2 expression was assessed by immunohistochemical staining of gastric biopsies, using mouse anti-human bcl-2 monoclonal antibodies. Autoimmune atrophic gastritis patients were younger, mainly females, with a significantly higher serum gastrin level than the H. pylori-associated atrophic gastritis group (P < 0.001). The bcl-2 was expressed in 10/20 (50%) of autoimmune atrophic gastritis patients, in 9/20 (45%) of H. pylori-associated atrophic gastritis patients (P = 0.73), and in 2/20 (10%) of controls. There was no correlation between bcl-2 expression and the presence of intestinal metaplasia (P = 0.35). Our findings confirm that H. pylori-associated atrophic gastritis and autoimmune atrophic gastritis are two different conditions, but with equal expression of bcl-2. Excessive expression of bcl-2 is found only in atrophic gastritis, but not in H. pylori antral gastritis without atrophy.

Gastrin increases mcl-1 expression in type I gastric carcinoid tumors and a gastric epithelial cell line that expresses the CCK-2 receptor

“…Gastrin has also been reported to increase the expression of bcl-2 and survivin in KATO III gastric adenocarcinoma cells (16). Increased immunohistochemical bcl-2 expression has been demonstrated in autoimmune as well as H. pylori associated atrophic gastritis (23) and in hypergastrinemia-associated ECL-cell gastric carcinoid tumors (1; 14). We also demonstrated increased bcl-2 expression in patients with atrophic gastritis and hypergastrinemia, but this bcl-2 expression appeared to occur predominantly in stromal and lymphoid cells rather than in ECL cells (figure 6).…”

“…IMGE-5) origin and gastrin-induced alterations in the expression of several members of the bcl-2 family of proteins have also previously been demonstrated (10; 11; 16; 31-33). Increased immunohistochemical expression of anti-apoptotic bcl-2 has also been demonstrated in biopsies obtained from human subjects with atrophic gastritis (23) and type I gastric carcinoid tumors (1).…”