Abstract
BackgroundHelicobacter pylori (H. pylori) causes gastritis and intestinal metaplasia (IM) that may evolve to gastric carcinoma. The objective of this study was to compare the profile of mucins in the progressive stages of H. pylori infected pre-neoplastic and neoplastic human gastric epithelium. We used a panel of monoclonal antibodies with well-defined specificities of MUC2, MUC5AC and MUC6 to characterize the expression pattern of mucins by immunohistochemistry.MethodsRUT and ELISA were down for H. pylori confirmation. Human gastric biopsy sections were stained using immunohistochemistry with MUC2, MUC5AC and MUC6 antibodies.ResultsMUC5AC was expressed in the superficial epithelium and the upper part of the gastric pits. MUC6 expression was detected in the lower part of the gastric glands. MUC2 was expressed in intestinal metaplasia, mostly in goblet cells. The mucin expression profile in the progressive stages of H. pylori infected human gastric epithelium allows the identification of intestinal metaplasia, which is characterized by a decreased expression of the gastric mucins (MUC5AC and MUC6) and de novo expression of MUC2.ConclusionIn conclusion, our results suggest that there is altered expression of MUC5AC and MUC6 together with the aberrant expression of MUC2 in intestinal metaplasia, during the process of gastric carcinogenesis. The present study indicates that the MUC2 mucin expression pattern is a reliable marker of intestinal metaplasia, which appears in the context of H. pylori infected individuals.
Highlights
Helicobacter pylori (H. pylori) causes gastritis and intestinal metaplasia (IM) that may evolve to gastric carcinoma
Expression pattern of MUC2, MUC5AC and MUC6 mucins in normal gastric mucosa MUC5AC was highly expressed in foveolar epithelium and mucous neck cells of antrum (> 75%, Fig. 1b; Fig. 3b; Table 2)
Expression of MUC6 was detected in the glands of the antrum (> 75%, Fig. 1c; Fig. 3c; Table 3) and MUC2 was not detected in normal gastric mucosa (Fig. 1a; Fig. 3a; Table 2)
Summary
Helicobacter pylori (H. pylori) causes gastritis and intestinal metaplasia (IM) that may evolve to gastric carcinoma. Helicobacter pylori colonizes human gastric mucosa and causes gastritis and intestinal metaplasia (IM), which may evolve towards gastric carcinoma [1,2,3]. H. pylori infection was established as a type I human carcinogen in IARC [4]; it was recently shown that the bacteria are capable of inducing gastritis, IM, and gastric carcinoma in Mongolian gerbils [5,6,7,8]. The normal gastric mucosa shows cell types specific expression of MUC1, MUC5AC, and MUC6, with first two mucins found in the superficial epithelium and MUC6 in the deep glands [22,25,26]. The normal gastric mucosa does not express MUC2 [25,27]
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