Local expressions of TGF-beta1, TGF-beta1RI, CTGF, and Smad-7 in Helicobacter pylori-associated gastritis

OBJECTIVE: Transforming growth-factor (TGF)-beta1 and Smad-7 play important roles in Helicobacter pylori (H. pylori)-associated gastritis. Connective tissue growth factor (CTGF) can facilitate the TGF-beta/Smad signaling by switching off Smad-7. The purpose of this study was to examine the in situ expressions of these cytokines in the gastric antrum with or without H. pylori infection. MATERIAL AND METHODS: Antral specimens from 166 patients (96 M, 70 F, median age 52 years, range 26 to 76 years) were used in this study. H. pylori infection status was determined by histological examination and (UBT) 13C]-urea breath test. Degrees of severity and activity of chronic gastritis were scored for all specimens. Immunohistochemistry was used to demonstrate local expressions of TGF-beta1, TGF-beta1 type 1 receptor (TGF-beta1RI), Smad-7, and CTGF in the gastric antrum. RESULTS: The results demonstrated that mononuclear cells (MNCs) in lamina propria were the major source of these cytokines. The number of MNCs stained with TGF-beta1, TGF-beta1RI, CTGF, and Smad-7 was significantly higher in H. pylori-positive patients than in H. pylori-negative patients. Furthermore, there was a positive correlation between these cytokine-producing MNCs and the severity of chronic gastritis. CONCLUSIONS: H. pylori infection is associated with increased expression of TGF-beta1, TGF-beta1RI, Smad-7, and CTGF in the gastric antrum. Our results also suggest that the feed-back loop consisting of TGF-beta1, Smad-7, and CTGF may play an important role in the pathogenesis of H. pylori-associated gastritis.