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We read the manuscript by Sonda et al1 recently published in Gut with great interest. The authors elegantly demonstrated that lack of peripheral serotonin (5-HT) in tryptophan hydroxylase 1 knockout (TPH1−/−) mice remarkably limited pancreatic damage and leucocyte infiltration during the early phase of cerulein-induced acute pancreatitis (AP) and identified 5-HT as an important regulator of zymogen secretion in acinar cells. Although the study was very comprehensive, the ductal function of TPH1−/− mice was not investigated, which might be another key player in this protection. Notably, 5-HT was shown to inhibit fluid and HCO3− secretion of pancreatic ductal epithelial cells,2 which play a pivotal role in pancreatic physiology and can influence the severity of AP.3 Thus, we investigated the possible alterations of pancreatic ductal secretion in TPH1−/− mice.
To achieve our aim, intralobular/interlobular pancreatic ducts were isolated from the pancreas of wild-type (TPH1+/+) and TPH1−/− mice. HCO3− secretion was measured by three different, but complementary methods using …
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