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Published Online First: 4 May 2005. doi:10.1136/gut.2005.066464
Gut 2006;55:152-157
Copyright © 2006 BMJ Publishing Group Ltd & British Society of Gastroenterology.

STOMACH

Helicobacter pylori eradication induces marked increase in H+/K+-adenosine triphosphatase expression without altering parietal cell number in human gastric mucosa

H Osawa, H Kita, H Ohnishi, H Hoshino, H Mutoh, Y Ishino, E Watanabe, K Satoh, K Sugano

Department of Internal Medicine, Division of Gastroenterology, Jichi Medical School, Kawachi, Tochigi, Japan

Correspondence to:
Dr H Osawa
Department of Internal Medicine, Division of Gastroenterology, Jichi Medical School, 3311–1 Yakushiji, Minamikawachi, Kawachi, Tochigi 329-0498, Japan; osawa{at}jichi.ac.jp

Background and aims: Gastric acid secretion is downregulated by Helicobacter pylori infection and upregulated after its eradication, but the mechanisms are still unclear. We examined the effects of H pylori eradication on the number of parietal cells and on expression of molecules functioning in acid secretion in the human gastric mucosa.

Methods: We enrolled 111 consecutive men with chronic gastritis induced by H pylori. Biopsy specimens were endoscopically obtained before and 12 weeks after successful eradication of H pylori and parietal cell numbers were counted. mRNA expression levels of H+/K+-adenosine triphosphatase (H+/K+-ATPase), anion exchanger 2, M3 muscarinic receptor, intrinsic factor, and interleukin 1ß were determined with a real time reverse transcriptase-polymerase chain reaction method. The severity of gastric atrophy was evaluated using the serum pepsinogen I/II ratio.

Results: No significant difference was observed in parietal cell numbers before and after H pylori eradication. Median mRNA expression levels of H+/K+-ATPase in the gastric mucosa increased 250-fold after H pylori eradication accompanied by attenuation of interleukin 1ß. A large increase in H+/K+-ATPase expression was observed even in patients with severe atrophic gastritis. In contrast, fold increases in mRNA expression levels, including intrinsic factor, anion exchanger 2, and M3 muscarinic receptor, after eradication therapy, were limited to 1.4, 2.3, and 2.5 times, respectively.

Conclusions: In the absence of alteration of parietal cell number, gastric H+/K+-ATPase mRNA expression was markedly restored after successful H pylori eradication, suggesting a central role for the restoration of H+/K+-ATPase expression in gastric acid secretion recovery after H pylori eradication.

Abbreviations: H+/K+-ATPase, H+/K+-adenosine triphosphatase; RT-PCR, reverse transcriptase-polymerase chain reaction; IL, interleukin; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; PPI, proton pump inhibitor

Keywords: H+/K+-ATPase; eradication therapy; parietal cell marker; Helicobacter pylori


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Mechanisms of increased acid secretion after eradication of Helicobacter pylori infection
E M El-Omar
Gut 2006 55: 144-146. [Extract] [Full Text] [PDF]

This article has been cited by other articles:

  • El-Omar, E M (2006). Mechanisms of increased acid secretion after eradication of Helicobacter pylori infection. Gut 55: 144-146 [Full Text]  

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