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Gastroenterology Section, Veterans Affairs Palo Alto Health Care System, Palo Alto 94304; and Division of Gastroenterology, Stanford University School of Medicine, Stanford, California 94305
Barrett's
esophagus (BE) results from acid and bile reflux and predisposes to
cancer. We investigated the effect of bile salts, with or without acid,
on cell proliferation in BE and assessed mechanism(s) involved. To
mimic physiological conditions, biopsies of esophagus, BE, and duodenum
were exposed to a bile salt mixture, either continuously or as a 1-h
pulse, and were compared with control media without bile salts (pH 7.4)
for 
24 h. Similar experiments were also performed with acidified
media (pH 3.5) combined with the bile salt mixture as a 1-h pulse. Cell
proliferation was assessed by a [3H]thymidine
incorporation assay with or without bisindolylmaleimide (BIM), a
selective protein kinase C inhibitor. Bile salt pulses enhanced cell
proliferation in BE without affecting cell proliferation in esophageal
or duodenal epithelia. In the presence of BIM, there was complete
obliteration of the bile salt-induced BE hyperproliferation. In
contrast, 1-h pulses of bile salts in combination with acid significantly inhibited proliferation in BE but had no effect on
esophagus or duodenum. We conclude that in BE explants, brief exposure
to bile salts, in the absence of acid, increases proliferation, whereas
exposure to a combination of bile salts and acid together inhibits proliferation.
gastroesophageal reflux disease; duodenogastric reflux
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