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Proton pump inhibitor modifies inflammatory reaction in human gastric mucosa infected by Helicobacter pylori
Author(s) -
Suzuki M.,
Suzuki H.,
Kitahora T.,
Miyazawa M.,
Nagahashi S.,
Suzuki K.,
Ishii H.
Publication year - 2002
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.16.s2.19.x
Subject(s) - helicobacter pylori , rabeprazole , gastroenterology , proton pump inhibitor , medicine , myeloperoxidase , lansoprazole , antrum , gastric mucosa , omeprazole , stomach , biopsy , pathology , inflammation
Aim: To examine whether proton pump inhibitors modify the production of oxygen‐derived free radicals and related cytokines in the human gastric mucosa infected with H. pylori . Methods: Thirty‐four H. pylori ‐positive peptic ulcer patients (23 gastric ulcer, 11 duodenal ulcer) were enrolled. Biopsy tissue samples were obtained endoscopically from the antrum and corpus. Tissue content of neutrophil myeloperoxidase (myeloperoxidase) and IL‐8 was measured by ELISA. Mucosal production of oxygen‐derived free radical was measured using luminol‐dependent chemiluminescence (ChL). A proton pump inhibitor (either lansoprazole 30 mg, omeprazole 20 mg, or rabeprazole 10 mg) was administered daily by mouth to all patients for 8 weeks. Endoscopic examination was then repeated, and biochemical analysis was performed. Results: Antral myeloperoxidase decreased significantly after proton pump inhibitor treatment (5.23 ± 7.00–2.76 ± 5.11 ng/mg, P < 0.02), but corpus myeloperoxidase was unchanged. IL‐8 was also modified by proton pump inhibitors and these changes were parallel to those of myeloperoxidase. Corpus ChL was significantly increased from 88.5 ± 69.8–159 ± 172 counts/10 s/mg after proton pump inhibitor treatment, whereas antrum ChL was not altered. H. pylori infection rate was decreased in the antrum as well as the corpus. Conclusions: Proton pump inhibitor treatment stimulated oxygen‐derived free radical production in the corpus mucosa.