Influence of gastritis on cyclooxygenase-2 expression before and after eradication of Helicobacter pylori infection.
OBJECTIVE
Helicobacter pylori infection causes chronic gastritis and induces cyclooxygenase (COX)-2 expression. The relationship between gastritis and COX-2 expression is not well understood, especially long after the organism has been eradicated. We designed a study to elucidate this relationship.


METHODS
Four endoscopic gastric biopsies from each of 118 H. pylori-infected subjects were assessed for COX-2 expression immunohistochemically, gastritis, by an updated Sydney System. In the 107 successfully eradicated subjects, the assessment was repeated once yearly, for 3 years.


RESULTS
After successful eradication, COX-2 expression was reduced significantly regardless of site. Atrophy improved significantly and intestinal metaplasia improved but not in the antrum greater curvature. After 1 year COX-2 expression was not significantly different in the epithelia with and without intestinal metaplasia. Correlation between COX-2 expression and neutrophil score in the antrum (r = 0.214, P = 0.042) and inflammation in the corpus (r = 0.234, P = 0.025) disappeared after eradication. COX-2 expression correlated well with atrophy and metaplasia before and after eradication. No significant reduction in COX-2 or improvement in gastritis was found in subjects with eradication failure.


CONCLUSIONS
H. pylori infection is associated with the enhancement of COX-2 expression in the gastric mucosa. Eradication therapy reduces COX-2 expression and hence may reduce the risk of cancer development.
Wambura
Casmir
C
Division of Diabetes, Digestive and Kidney Diseases, Department of Clinical Molecular Medicine, Kobe University Graduate School of Medicine, Japan.
Aoyama
Nobuo
N
Shirasaka
Daisuke
D
Kuroda
Kohei
K
Maekawa
Shuji
S
Ebara
Shigeyuki
S
Watanabe
Yoshinori
Y
Tamura
Takao
T
Kasuga
Masato
M
D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000328:Adult; D000368:Aged; D051546:Cyclooxygenase 2; D005260:Female; D005500:Follow-Up Studies; D005753:Gastric Mucosa / Q000201:enzymology* / Q000276:immunology; D005756:Gastritis / Q000188:drug therapy / Q000201:enzymology* / Q000276:immunology; D005773:Gastroscopy; D016481:Helicobacter Infections / Q000188:drug therapy / Q000201:enzymology* / Q000276:immunology; D016480:Helicobacter pylori; D006801:Humans; D064747:Lansoprazole; D008297:Male; D008565:Membrane Proteins; D008875:Middle Aged; D018375:Neutrophil Activation; D009853:Omeprazole / Q000031:analogs & derivatives* / Q000627:therapeutic use; D011451:Prostaglandin-Endoperoxide Synthases / Q000032:analysis / Q000378:metabolism*; D054328:Proton Pump Inhibitors; D018709:Statistics, Nonparametric; D013997:Time Factors
D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D008565:Membrane Proteins; D054328:Proton Pump Inhibitors; D064747:Lansoprazole; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; D009853:Omeprazole