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

Abstract:

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.

journal_name

Scand J Gastroenterol

authors

von Bothmer C,Edebo A,Lönroth H,Olbe L,Pettersson A,Fändriks L

doi

10.1080/003655202317316024

subject

Has Abstract

pub_date

2002-04-01 00:00:00

pages

404-8

issue

4

eissn

0036-5521

issn

1502-7708

journal_volume

37

pub_type

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