Eradication therapy of Helicobacter pylori directly induces apoptosis in inflammation-related immunocytes in the gastric mucosa--possible mechanism for cure of peptic ulcer disease and MALT lymphoma with a low-grade malignancy.
OBJECTIVE
A possibility that the eradication therapy not only eliminates Helicobacter pylori (H. pylori) but also influences some factors regulating pathological changes in the gastric mucosa should be taken into consideration from some phenomena. Such as non-recurrent cases of peptic ulcer long-term in spite of unsuccessful anti-H. pylori eradication therapy and the effectiveness of eradication therapy for mucosa-associated lymphoid tissue with a low-grade malignancy except stomach. We hypothesized and investigated that antibiotic treatment for elimination of H. pylori might directly affect inflammatory cells to induce apoptosis in them and protect against pathological changes of gastric mucosa.


METHODS
Subjects consisted of twenty-one patients with chronic gastritis. All were H. pylori positive and we investigated the effects of eradication therapy of H. pylori on inflammation-related immunocytes in the gastric mucosa of patients with chronic gastritis caused by H. pylori isolated mononuclear leukocytes which were taken from the patients and were examined for apoptosis-related morphological changes and DNA fragmentation before and after the therapy. Eradication therapy of H. pylori was performed by lansoprazole 30 mg/day, amoxicillin 1500 mg/day and clarithromycin 400 mg/day for one week.


RESULTS
After the H. pylori eradication therapy, regardless of its effect on H. pylori status, marked vacuolation and degeneration were observed in mononuclear leukocytes in the gastric mucosa with a concomitant enhancement of nuclear DNA fragmentation.


CONCLUSIONS
This observation suggests that H. pylori eradication therapy itself induces apoptosis in mononuclear leukocytes in the gastric mucosa.
Ohara
Tadashi
T
Department of Internal Medicine, Chiba Hospital, Tokyo Dental College, Ichikawa General Hospital, Chiba, Japan. jlohara@sm.rim.or.jp
Kanoh
Yuhsaku
Y
Higuchi
Kazuhide
K
Arakawa
Tetsuo
T
Morisita
Testsuo
T
D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000658:Amoxicillin / Q000627:therapeutic use*; D000897:Anti-Ulcer Agents / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects*; D002908:Chronic Disease; D017291:Clarithromycin / Q000627:therapeutic use*; D004359:Drug Therapy, Combination / Q000627:therapeutic use*; D005260:Female; D005753:Gastric Mucosa / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D005756:Gastritis / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D016481:Helicobacter Infections / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D016480:Helicobacter pylori / Q000187:drug effects; D006801:Humans; D064747:Lansoprazole; D007958:Leukocyte Count; D018442:Lymphoma, B-Cell, Marginal Zone / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009853:Omeprazole / Q000031:analogs & derivatives / Q000627:therapeutic use*; D010437:Peptic Ulcer / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D054328:Proton Pump Inhibitors; D013602:T-Lymphocytes, Cytotoxic / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D016896:Treatment Outcome
D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000897:Anti-Ulcer Agents; D054328:Proton Pump Inhibitors; D064747:Lansoprazole; D000658:Amoxicillin; D017291:Clarithromycin; D009853:Omeprazole