Helicobacter pylori infection inhibits antral mucosal nitric oxide production in humans.

BACKGROUND

Inducible NO synthase expression is upregulated in H. pylori-infected gastric mucosa, suggesting increased NO synthesis as part of a host defense reaction. This study investigates actual NO production in the human antrum in situ.

METHODS

Gastroscopy with antral biopsy sampling and intragastric tonometric NO assessments were performed on H. pylori-positive and -negative volunteers. The antral mucosal specimens were analyzed with regard to inducible NO synthase (Western blotting) and the presence of the endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA) as well as L-arginine.

RESULTS

Mucosal expression of inducible NO synthase was markedly increased in H. pylori infected subjects compared to noninfected ones. The ratio between the tissue contents of L-arginine and asymmetric dimethylarginine was considerably lower in the infected group. Antral output of NO was similar in the two groups during baseline conditions. Following intragastric L-arginine exposure. the antral NO production in controls was unaltered (from 442 ppb +/- 104 to 286 ppb +/- 94), whereas it increased (from 524 ppb +/- 162 to 1066 ppb +/- 274) in the infected individuals.

CONCLUSIONS

The study confirms that NO synthase expression is increased in H. pylori-infected antral mucosa. However, NO synthesis is restricted owing to the presence of pathogen-induced competitive NO synthase inhibitors such as methylated arginines.