Helicobacter pylori stimulates pepsin secretion from isolated rabbit gastric glands.
In man, type-B gastritis caused by Helicobacter pylori has been associated with both increased serum pepsinogen in the presence of hypochlorhydria and increased levels of gastric pepsin. We investigated the effect of H. pylori on pepsinogen secretion in vitro and found that a sonicated preparation of H. pylori increased pepsinogen secretion from isolated rabbit gastric glands. This increase was significant after 5 min (p = 0.001), and maximum secretion was obtained after 30 min of incubation. The effect was additive to the secretion achieved by stimulation with carbachol at 10(-4) M plus 10(-4) isobutylmethylxanthine or 10(-8) M cholecystokinin. There was no detectable stimulation of pepsinogen synthesis by 2 h. Lactate dehydrogenase (LDH) release was assayed as an index of cell damage, and no significant LDH release was noted. The secretory factor in the H. pylori sonicate is inhibited by boiling, unaffected by heating at 60 degrees C for 30 min, dialysable, and inactivated by pronase. These data suggest that H. pylori stimulates pepsinogen secretion by a mechanism different from that of other tested stimulants. H. pylori-stimulated pepsinogen release may be a factor in the etiology of type-B gastritis and peptic ulcers.
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Evans Memorial Dept. of Clinical Research, Boston University Medical Center, Massachusetts.
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D000704:Analysis of Variance; D000818:Animals; D005753:Gastric Mucosa / Q000201:enzymology*; D016480:Helicobacter pylori / Q000502:physiology*; D008297:Male; D010434:Pepsin A / Q000378:metabolism*; D010437:Peptic Ulcer / Q000201:enzymology / Q000382:microbiology*; D011817:Rabbits
D010434:Pepsin A