Effects of Helicobacter pyloriinfection on gastric acid secretion and serum gastrin levels in Mongolian gerbils (original) (raw)

Effects of _Helicobacter pylori_infection on gastric acid secretion and serum gastrin levels in Mongolian gerbils

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  1. M Takashima,
  2. T Furuta,
  3. H Hanai,
  4. H Sugimura,
  5. E Kaneko
  6. First Department of Medicine, First Department of Pathology, and Department of Endoscopic and Photodynamic Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan
  7. Dr M Takashima, First Department of Medicine, Hamamatsu University School of Medicine, 3600, Handa-cho, Hamamatsu, 431–3192, Japan.takam{at}h7.dion.ne.jp

Abstract

BACKGROUND AND AIMS Body gastritis caused by Helicobacter pylori infection appears to inhibit gastric acid secretion. The aim of this study was to determine the effects of_H pylori_ infection on gastric acid secretion and clarify its mechanisms with reference to interleukin 1β (IL-1β).

METHODS (1) Mongolian gerbils were inoculated orally with H pylori. Before, six, and 12 weeks after inoculation, serum gastrin levels, gastric acid output, and IL-1β mRNA levels in the gastric mucosa were determined. Pathological changes were also determined according to the updated Sydney system. (2) Effects of recombinant human IL-1 receptor antagonist (rhIL-1ra) on gastric acid output and serum gastrin levels were also determined.

RESULTS (1) Scores for activity and inflammation of gastritis and serum gastrin levels were significantly increased, and gastric acid output was significantly decreased six and 12 weeks after inoculation with_H pylori._ IL-1β mRNA levels in the gastric mucosa were also elevated six and 12 weeks after inoculation with_H pylori_. (2) Acid output and serum gastrin levels in the infected groups returned to control levels after rhIL-1ra injection.

CONCLUSIONS Gastric acid secretion is decreased and serum gastrin levels are increased in Mongolian gerbils infected with H pylori. This change in gastric acid secretion appears to be mediated by IL-1β induced by H pylori infection.

IL-1β
interleukin 1β
rhIL-1ra
recombinant human IL-1 receptor antagonist
CFU
colony forming units
PCR
polymerase chain reaction

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