HELICOBACTER-PYLORI STIMULATES GASTRIC-ACID SECRETION VIA PLATELET-ACTIVATING-FACTOR

Platelet activating factor (PAF) is a phospholipid mediator known as p otent ulcerogenic agent but its physiological role is still unknown in the gastrointestinal tract. Lyse PAF the immediate PAF procursor has no deleterious effect in the gastrointestinal tract. We have previousl y reported that lyse PAF is produced by gastric mucosa in basal condit ion and in response to gastrin in healthy men. Helicobacter pylori met abolises lyse PAF to produce PAF. The aim was to study the effect of P AF on the gastric acid secretion. Isolated rabbit glands were used as a model and acid secretion was assessed by (C-14) Aminopyrine (AP) upt ake. PAF and histamine stimulated AP accumulation time- and dose-depen dently, PAF-induced AP accumulation was supressed by omeprazole and Fu ra 2. BN50727 a specific PAF antagonist inhibited PAF-induced AP accum ulation. The presence of a PAF receptor transcript was investigated by reverse transcriptase polymerase chain reaction (RT-PCR) from total m RNA using two primers in which oligonucleotides were synthetized from the human leucocyte PAF receptor cDNA. A single RT-PCR band of the tra nscript with expected size was detected in the crude isolated cell fra ction. These results and others from our laboratory suggest that PAF s timulates gastric acid secretion via specific receptor on the parietal cells and H. pylori produces PAF which may induce mucosal injury dire ctly or indirectly via acid pathway.