Role of transforming growth factor β1 in the development of atrophic gastritis / 北京大学学报(医学版)

ABSTRACT

Objective:To investigate the role of transforming growth factor β1 (TGFβ1) in the development of Helicobacter pylori ( H. pylori)-associated non-metaplastic atrophic gastritis. Methods:The expressions of TGFβ1, CD68 and smooth muscle actin(SMA) were detected immunohistochemically in 10 patients with mild non-atrophic gastritis, 30 patients with mild non-metaplastic atrophic gastritis, and 32 patients with severe non-metaplastic atrophic gastritis having H. pylori infecion. Meanwhile, three cases of mild non-atrophic gastritis and 4 cases of severe non-metaplastic atrophic gastritis were observed with electron microscope. Results: The count of TGFβ1 positive cells per high-power field (HPF) in severenon-metaplastic atrophic gastritis group (53±22 ) was significantly higher than that in mild non-atrophic gastritis group(22±/HPF) and mild non-atrophic gastritis group(0-3/HPF, P＜0.01). The count of CD68 positive cells in severe non-metaplastic atrophic gastritis group (23±7/HPF) was significantly higher than that in mild non-atrophic gastritis group (13±/HPF) and mild non-atrophic gastritis group (0-3/HPF, P＜0. 01). Correlation analysis showed that the expressions of TGFβ1 and CD68 had a moderate correlation in each group ( r = 0. 634, P＜ 0. 01; r = 0. 699, P＜ 0. 01). Compared with mild non-atrophic gastritis, SMA-positive myofibroblasts and smooth muscle cells in the lamina propria increased in mild and severe non-metaplastic atrophic gastritis. Ultrastructurally, the proliferation of fibroblasts in gastric lamina propria was observed in mild non-atrophic gastritis, while the proliferation of fibroblasts and presence of myofibroblasts could be observed in mild non-metaplastic atrophic gastritis, and there was a parallel phenomenon between myofibroblasts and fibroblasts, as well as smooth muscle cells.Conclusion: Our findings indicate that TGFβ1 expression increases with severity of H. pylori-associated non-metaplastic atrophic gastritis, suggesting that TGFβ1 might play an important role in the development of non-metaplastic atrophic gastritis.