This study aimed at the relationship of helicobacter pylori infection to gastric carcinoma pathogenesis. Forty-nine serum samples from patients with gastric and duodenal ulcer and 20 serum sample from normal subjects were collected for the assessment of serum gastrin by radioimmunoassay (RIA) and serum IgG, IgA and IgM antibodies against H. pylori by ELISA respectively. The patients, serum samples were divided into four groups for observations on whether the sera would affect the cell proliferation of HAC803 derived from human gastric carcinoma and of HT29 from human colonic carcinoma cultured in vitro. The cell proliferation was determined by MIT assay. The results showed that the level of serogastrin in gastric and duodenal ulcer was significantly higher than that in normal control (139.6 +/- 38.17 pg/ml vs 63.12 +/- 28.7 pg/ml, P < 0.01). As for the sera of ulcer subjects, the highest anti-HpIgG group (group A) and the highest anti-Hp IgA group (group B) displayed a significantly enhanced cell proliferation of human gastric carcinoma (P < 0.05), especially group B. But all the four groups had less significant increase in cell proliferation of human colonic carcinoma (P > 0.05). These findings indicate that, in the highest anti-HpIgG group and the highest IgA group of the peptic ulcer subjects infected by H. pylori, the sera can enhance cell proliferation of gastric carcinoma, however the role is less associated with serum gastrin.
Antibodies, Bacterial Cell Division