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Gastroenterology Section, Veterans Affairs Palo Alto Health Care System, Palo Alto 94304; and Division of Gastroenterology and Hepatology, Stanford University, Stanford, California 94305
Barrett's esophagus (BE) results from acid and bile reflux and predisposes to cancer. To further understand the mechanisms of acid- and bile-induced hyperproliferation in BE, we investigated the release of PGE2 in response to acid or bile salt exposure. Biopsies of esophagus, BE, and duodenum were exposed to a bile salt mixture as a 1-h pulse and compared with exposure to pH 7.4 for up to 24 h, and PGE2 release, cyclooxygenase-2 (COX-2), and protein kinase C (PKC) expression were compared. Similar experiments were also performed with acidified media (pH 3.5) alone, in the presence or absence of bisindolylmaleimide (BIM), a selective PKC inhibitor, and NS-398, a COX-2 inhibitor. One-hour pulses of bile salts or acid significantly enhanced proliferation, COX-2 expression, and PGE2 release in BE. In contrast, the combination pulse of acid and bile salts had no such effect. Treatment with either BIM or NS-398 led to a dramatic decrease in PGE2 release in BE explants and a suppression of proliferation. The acid- or bile salt-mediated hyperproliferation is related to PGE2 release. Acid- and bile salt-induced induction of COX-2 and PKC may explain, at least in part, the tumor-promoting effects of acid and bile in BE.
acid; bile salts; gastroesophageal reflux disease; protein kinase C; cyclooxygenase-2; prostaglandins; duodenogastric reflux
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