The Kurume medical journal · 2023
Influence of Helicobacter Pylori Infection on Hepcidin Expression in the Gastric Mucosa.
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Nishigaki Yuki, Sato Yuichi, Sato Hiroki, Iwafuchi Mitsuya, Terai Shuji
Аннотация
BACKGROUND: Hepcidin is an antimicrobial peptide and a key hormone involved in iron homeostasis. Hepcidin level is elevated in the serum during the course of Helicobacter pylori infection and hepcidin is considered to contribute to iron deficiency anemia. However, it is unclear whether H. pylori infection influences hepcidin expression in the gastric mucosa.
METHOD: In this study, 15 patients with H. pylori-infected nodular gastritis, 43 patients with H. pylori-infected chronic gastritis, and 33 patients without H. pylori infection were enrolled. Endoscopic biopsy, and histological and immunohistochemical analysis were performed to evaluate the expression of hepcidin and its distribution in the gastric mucosa.
RESULT: Hepcidin was strongly expressed in the lymph follicles of patients with nodular gastritis. The detection rates of gastric hepcidin-positive lymphocytes in patients with nodular gastritis and chronic gastritis were significantly higher than that without H. pylori infection. Moreover, regardless of the H. pylori infection status, hepcidin was expressed in the cytoplasm and intracellular canaliculi of gastric parietal cells.
CONCLUSION: Hepcidin is expressed at a steady state in gastric parietal cells, and H. pylori infection may induce hepcidin expression in lymphocytes present in the gastric mucosal lymphoid follicles. This phenomenon may be associated with systemic hepcidin overexpression and iron deficiency anemia in patients with H. pylori-infected nodular gastritis.
METHOD: In this study, 15 patients with H. pylori-infected nodular gastritis, 43 patients with H. pylori-infected chronic gastritis, and 33 patients without H. pylori infection were enrolled. Endoscopic biopsy, and histological and immunohistochemical analysis were performed to evaluate the expression of hepcidin and its distribution in the gastric mucosa.
RESULT: Hepcidin was strongly expressed in the lymph follicles of patients with nodular gastritis. The detection rates of gastric hepcidin-positive lymphocytes in patients with nodular gastritis and chronic gastritis were significantly higher than that without H. pylori infection. Moreover, regardless of the H. pylori infection status, hepcidin was expressed in the cytoplasm and intracellular canaliculi of gastric parietal cells.
CONCLUSION: Hepcidin is expressed at a steady state in gastric parietal cells, and H. pylori infection may induce hepcidin expression in lymphocytes present in the gastric mucosal lymphoid follicles. This phenomenon may be associated with systemic hepcidin overexpression and iron deficiency anemia in patients with H. pylori-infected nodular gastritis.