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Helicobacter pylori infection: physiopathologic implication of N alpha-methyl histamine

A Courillon-Mallet1, J M Launay, A M Roucayrol

  • 1Department of Gastroenterology, Hôpital de Villenuve Saint Georges, France.

Gastroenterology
|April 1, 1995
PubMed
Abstract

Insights

Helicobacter pylori infection produces N alpha-methyl histamine (N alpha-MeHA) in the stomach. This compound may reduce histamine and somatostatin levels by activating histamine H3 receptors.

Area of Science:

  • Gastroenterology and Molecular Biology
  • Microbiology

Background:

  • Helicobacter pylori infection is associated with changes in gastric mucosal function.
  • N alpha-methyl histamine (N alpha-MeHA), a histamine metabolite and H3 receptor agonist, was previously detected in H. pylori-infected gastric mucosa.

Purpose of the Study:

  • To investigate the origin of gastric N alpha-MeHA in H. pylori-infected subjects.
  • To determine the effects of N alpha-MeHA on gastric histamine and somatostatin levels.

Main Methods:

  • Comparative analysis of N alpha-MeHA content, N alpha-histamine methyltransferase activity, histamine and somatostatin levels, and histidine decarboxylase activity in gastric biopsy specimens from infected and non-infected individuals.
  • Assay of these parameters in cultured H. pylori strains.
  • Radioligand binding studies using [3H]N alpha-MeHA to identify specific binding sites.

Main Results:

  • Gastric histamine, somatostatin, and histidine decarboxylase activity were reduced in H. pylori-infected patients and normalized post-treatment.
  • N alpha-MeHA and its synthetic enzyme activity were significantly higher in infected patients and H. pylori strains, decreasing after eradication.
  • [3H]N alpha-MeHA specifically bound to gastric mucosa, identifying H3 receptors, with binding correlated to somatostatin and histidine decarboxylase levels.

Conclusions:

  • Helicobacter pylori is the primary source of gastric N alpha-MeHA.
  • N alpha-MeHA may suppress histidine decarboxylase activity and somatostatin content via H3 receptor activation in the gastric mucosa.

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