Abstract
Background: The updated model for the mechanism of gastric carcinogenesis demonstrates that Helicobacter pylori (H. pylori) is a risk factor in every step of the process. The expression of certain gastric mucins is altered by H. pylori infection in adult patients. The aim of our research was to assess the impact of H. pylori infection on the expression of secretory mucins in the pediatric antral mucosa. Methods: Slides were stained with monoclonal antibodies for MUC5AC, MUC6 and MUC2, digitalized and scored using both a semiquantitative and a quantitative approach. Results: The expression of MUC5AC was significantly lower in infected children. Also, MUC2 expression was more pronounced in infected children. MUC6 expression did not differentiate between infected and noninfected children. Additionally, the presence of chronic inflammation significantly altered the expression of MUC6 and MUC2. The expression of MUC6 was significantly higher in patients with gastric atrophy. Conclusion: The minor differences in mucin expression at distinct ages might stem from different H. pylori exposure periods. Further research is needed to determine the particular patterns of expression according to age and to evaluate the effects of the interaction between H. pylori and mucins in the progression of the gastric carcinogenesis cascade.
Highlights
Helicobacter pylori is the etiological agent of the most common chronic infection in the world, both among adults and children [1]
The human gastric mucosa expresses both membrane-bound (MUC1), and secreted mucins (MUC5AC and MUC6); MUC5AC is secreted by the superficial cells, and MUC6 is secreted in the gastric glands, both of them being expressed in the normal gastric mucosa [5]
We compared the two methods by which we evaluated the immunohistochemical expression of mucins and we found a weak correlation between the immunoreactive score (IRS) score and the optical density score (ODS) score determined in the superficial/foveolar region of the antral mucosa for the expression of MUC5AC (r = 0.20, p < 0.001), and between the IRS score and the ODS score determined in the glandular region of the antral mucosa for the expression of MUC6 (r = 0.01, p = 0.93)
Summary
Helicobacter pylori is the etiological agent of the most common chronic infection in the world, both among adults and children [1]. The updated model for the mechanism of gastric carcinogenesis showed that H. pylori is present at the debut but it is an etiological factor in every step of the cascade [3]. The updated model for the mechanism of gastric carcinogenesis demonstrates that Helicobacter pylori (H. pylori) is a risk factor in every step of the process. The expression of certain gastric mucins is altered by H. pylori infection in adult patients. Further research is needed to determine the particular patterns of expression according to age and to evaluate the effects of the interaction between H. pylori and mucins in the progression of the gastric carcinogenesis cascade
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