Helicobacter Pylori
Copyright ©The Author(s) 2005. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jul 21, 2005; 11(27): 4148-4153
Published online Jul 21, 2005. doi: 10.3748/wjg.v11.i27.4148
Enhanced plasma ghrelin levels in Helicobacter pylori-colonized, interleukin-1-receptor type 1-homozygous knockout (IL-1R1-/-) mice
Yuka Abiko, Hidekazu Suzuki, Tatsuhiro Masaoka, Sachiko Nomura, Kumiko Kurabayashi, Hiroshi Hosoda, Kenji Kangawa, Toshifumi Hibi
Yuka Abiko, Hidekazu Suzuki, Tatsuhiro Masaoka, Sachiko Nomura, Kumiko Kurabayashi, Toshifumi Hibi, Department of Internal Medicine and Center for Integrated Medical Research, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan
Hiroshi Hosoda, Kenji Kangawa, Department of Biochemistry, National Cardiovascular Center Research Institute, Suita, Osaka 565-8565, Japan
Author contributions: All authors contributed equally to the work.
Supported by a Grant-in-Aid for Scientific Research C (2) from the Japan Society for the Promotion of Science (JSPS) (15590686, to H.S.), and a grant from the Keio University School of Medicine
Correspondence to: Hidekazu Suzuki, MD, PhD, Assistant Professor, Department of Internal Medicine, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. hsuzuki@sc.itc.keio.ac.jp
Telephone: +81-3-5363-3914 Fax: +81-3-5363-3967
Received: October 14, 2004
Revised: November 23, 2004
Accepted: November 29, 2004
Published online: July 21, 2005
Abstract

AIM: Ghrelin is an endogenous ligand for the growth hormone secretagogue receptor, and it plays a role in stimulating the growth hormone secretion, food intake, body weight gain and gastric motility. Eradication of

Helicobacter pylori (H pylori) was shown to be associated with increase of the body weight. On the other hand, H pylori infection evokes the release of gastric IL-1β. The present study was designed to investigate the involvement of the gastric IL-1 signal in the ghrelin dynamics in H pylori-colonized mice.

METHODS: Twelve-week-old female IL-1-receptor type 1-homozygous-knockout mice (IL-1R1-/-) and their wild-type littermates (WT) were orally inoculated with H pylori (Hp group), while other cohorts received oral inoculation of culture medium (Cont group). Thirteen weeks after the inoculation, the mice were examined. The plasma and stomach ghrelin levels and the gastric preproghrelin mRNA were measured.

RESULTS: Although the WT mice with H pylori infection showed a significantly decreased body weight as compared with that of the animals without H pylori infection, H pylori infection did not influence the body weight of the IL-1R1-knockout (IL-1R1-/-) mice. In the H pylori-infected IL-1R1-/- mice, the total and active ghrelin levels in the plasma were significantly increased, and the gastric ghrelin level was decreased. No significant differences were noted in the gastric preproghrelin mRNA expression.

CONCLUSION: Ghrelin secretion triggered by H pylori infection might be suppressed by IL-1β, the release of which is also induced by the infection, resulting in the body weight loss of mice with H pylori infection.

Keywords: Ghrelin; H pylori; IL-1; Body weight; Myelo-peroxidase