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Acta Physiologica 2008; Volume 193, Supplement 664
Scandinavian Physiological Society’s Annual Meeting 2008
8/15/2008-8/17/2008
Oulu, Finland
ORAL BACTERIA REGULATE GASTRIC MUCOSAL DEFENSE VIA BIOACTIVATION OF DIETARY NITRATE
Abstract number: P40
PETERSSON1 J, SCHREIBER1 O, PHILLIPSON1 M, ROOS1 S, JANSSON1 EÅ, LUNDBERG1 J, HOLM1 L
1Dept. of Medical Cell Biology, Uppsala University, Uppsala, Sweden
Background and Aims:
Dietary nitrate enhances gastric mucosal defense by luminal NO production, as oral bacteria reduce salivary nitrate to nitrite, which is further reduced to bioactive nitric oxide in the acidic stomach. The bacterial conversion of nitrate to nitrite is a crucial step in the formation of the protective NO in the stomach. We evaluated the importance of oral bacteria during nitrate supplementation on gastric mucosal defense in rats and mice.
Methods:
Regular drinking water or nitrate supplemented water was given to the animals for one week. The oral bacterial flora was suppressed with an antiseptic mouth spray twice daily during this period. Intragastric NO and plasma nitrite were measured by chemiluminescence. The thickness of the gastric mucus layers was measured in vivo with the animal's stomach exteriorized for intravital microscopy. Additionally, the stomach was challenged with diclofenac and the gastric levels of P-selectin were quantified using the dual labeled antibody technique.
Results:
Nitrate supplementation resulted in increased levels of intragastric NO and plasma nitrite. These effects were strongly reduced in animals with a suppressed oral flora. Nitrate supplementation increased the thickness of the adherent gastric mucus layer. This protective effect was totally absent in mouth-sprayed animals. Dietary nitrate protected against diclofenac induced damage and this protection was abolished if the oral flora was reduced.
Conclusions:
The formation of intragastric NO from dietary nitrate is critically dependent on oral bacteria. Without these bacteria, the gastroprotective role of nitrate is abolished.
To cite this abstract, please use the following information:
Acta Physiologica 2008; Volume 193, Supplement 664 :P40