Proton pump inhibitor modifies inflammatory reaction in human gastric mucosa infected by Helicobacter pylori
M Suzuki1, H Suzuki, T Kitahora
1Division of Gastroenterology, National Tokyo Medical Center, Meguro-ku, Tokyo, Japan. msuzuki@ntmc.hosp.go.jp
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.
Insights
Proton pump inhibitors altered oxygen-derived free radical production in H. pylori-infected gastric mucosa. While antral inflammation markers decreased, corpus free radical production increased following treatment.
Area of Science:
- Gastroenterology
- Oncology
- Pharmacology
Background:
- Helicobacter pylori infection is a major cause of peptic ulcer disease.
- Proton pump inhibitors (PPIs) are widely used to treat acid-related disorders.
- The impact of PPIs on mucosal inflammation and oxidative stress in H. pylori infection requires further investigation.
Purpose of the Study:
- To investigate the effect of proton pump inhibitors on oxygen-derived free radical production and related cytokines in H. pylori-infected human gastric mucosa.
Main Methods:
- Thirty-four H. pylori-positive peptic ulcer patients received PPIs (lansoprazole, omeprazole, or rabeprazole) for 8 weeks.
- Gastric biopsy samples were analyzed for myeloperoxidase (MPO), IL-8, and oxygen-derived free radical production (chemiluminescence).
- Measurements were taken before and after PPI treatment.
Main Results:
- PPI treatment significantly reduced antral MPO and IL-8 levels.
- Corpus MPO and IL-8 levels remained unchanged.
- Corpus oxygen-derived free radical production significantly increased after PPI treatment.
- H. pylori infection rates decreased in both antrum and corpus.
Conclusions:
- Proton pump inhibitor treatment appears to stimulate oxygen-derived free radical production in the gastric corpus mucosa.
- PPIs may differentially affect inflammatory pathways in the antrum versus the corpus.
- Further research is needed to elucidate the clinical implications of these findings.
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