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Altered gastrin regulation in mice infected with Helicobacter felis
E J Dial1, L R Hall, J J Romero
1Department of Integrative Biology, Pharmacology, and Physiology, The University of Texas-Houston Medical School, 77225, USA.
Abstract:
Altered gastrin expression associated with Helicobacter pylori infection may contribute to the pathogenesis of peptic ulcer disease or gastric cancer in man, but gastrin has not been investigated in a murine model of Helicobacter infection. C57BL/6 mice were inoculated with Helicobacter felis and examined after 4-21 weeks for G and D cell numbers, antral gastrin and somatostatin mRNA, and luminal pH. In H. felis-infected mice, gastrin mRNA declined at four and six weeks after infection to 57% and 23%, respectively, of uninfected control values. Concurrently, somatostatin mRNA showed no change at four weeks and a modest 25% decrease at six weeks after infection. Similar reductions were noted in G and D cell numbers, resulting in a decrease in the G/D cell ratio after mice were infected with H. felis. Infected animals also showed a loss of parietal and chief cells, and an increased gastric pH. H. felis infection in C57BL/6 mice leads to an early suppression of G cell number and gastrin mRNA. These changes precede an alteration in somatostatin cell number and mRNA and, coupled with reductions in parietal and chief cells, may contribute both to severe impairment of gastric acid output and the potential for carcinogenic processes.
Insights
Helicobacter felis infection in mice suppresses gastrin production and G cell numbers early on. This may impair gastric acid and increase cancer risk.
Area of Science:
- Gastroenterology
- Microbiology
- Pathology
Background:
- Altered gastrin expression is linked to peptic ulcers and gastric cancer.
- Gastrin's role in Helicobacter infection pathogenesis remains unclear in murine models.
Purpose of the Study:
- Investigate the impact of Helicobacter felis infection on gastrin and somatostatin expression in C57BL/6 mice.
- Determine the effects on gastric cell populations and acidity.
Main Methods:
- C57BL/6 mice were infected with Helicobacter felis.
- Examined G and D cell numbers, gastrin and somatostatin mRNA levels, and gastric pH at 4-21 weeks post-infection.
Main Results:
- Helicobacter felis infection led to significant early declines in gastrin mRNA and G cell numbers.
- Somatostatin mRNA and D cell numbers showed delayed and less pronounced reductions.
- Infected mice exhibited parietal and chief cell loss, increased gastric pH, and a decreased G/D cell ratio.
Conclusions:
- Early suppression of gastrin and G cells by H. felis precedes somatostatin changes.
- These alterations, along with cell loss and increased pH, may contribute to impaired gastric acid secretion and carcinogenic processes.