Article Text
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 ofH 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 withH pylori. IL-1β mRNA levels in the gastric mucosa were also elevated six and 12 weeks after inoculation withH 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.
- Helicobacter pylori
- interleukin 1β
- Mongolian gerbils
- gastric acid
- gastrin
Abbreviations used in this paper
- IL-1β
- interleukin 1β
- rhIL-1ra
- recombinant human IL-1 receptor antagonist
- CFU
- colony forming units
- PCR
- polymerase chain reaction
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Abbreviations used in this paper
- IL-1β
- interleukin 1β
- rhIL-1ra
- recombinant human IL-1 receptor antagonist
- CFU
- colony forming units
- PCR
- polymerase chain reaction