They discovered that acid, on the other hand, didn't largely influence the change from one cell type to another.
While previous research established that reflux components encouraged the development of intestinal tissue in the esophagus that alone was never enough to produce the changes that led to Barrett's.
"The main leap this study makes is that normal esophageal cell growth must be turned off and intestinal cell growth must be turned on in order for the disease to take hold," noted Peters, who is president elect of the International Society of Diseases of the Esophagus. "We found that bile promotes both processes."
Study author Tony E. Godfrey, Ph.D., says the findings make perfectly good sense. "In people with Barrett's, the inside of the esophagus looks like the inside of the intestine. Bile is normally found in the intestinal environment, so when stem cells in the esophagus are exposed to bile that is what they change to."
According to Godfrey, a research associate professor in the Department of Surgery, the lining of the esophagus is shed and replaced on a regular basis, so blocking bile's ability to thwart the production of normal esophageal cells may be one potential treatment strategy. Currently, the only way to stop all reflux components, including bile, is to surgically reconstruct the faulty barrier between the esophagus and the stomach.
The team performed the first-ever analysis of all genes that are turned on and off in normal esophageal cells exposed chronically to bile or acid. The fi
|Contact: Emily Boynton|
University of Rochester Medical Center