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Pancreatic epithelial fluid and bicarbonate secretion is significantly elevated in the absence of peripheral serotonin
  1. József Maléth1,
  2. Tamara Madácsy1,
  3. Petra Pallagi1,
  4. Anita Balázs1,
  5. Viktória Venglovecz2,
  6. Zoltán Rakonczay Jr1,
  7. Péter Hegyi1,3
  1. 1First Department of Medicine, University of Szeged, Szeged, Hungary
  2. 2Department of Pharmacology and Pharmacotherapy, University of Szeged, Szeged, Hungary
  3. 3MTA-SZTE Momentum Translational Gastroenterology Research Group, University of Szeged, Szeged, Hungary
  1. Correspondence to Professor Péter Hegyi, First Department of Medicine, Faculty of Medicine, University of Szeged, P.O. Box 427, Szeged H-6701, Hungary; hegyi.peter{at}med.u-szeged.hu

https://doi.org/10.1136/gutjnl-2015-309776

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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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    Footnotes

    • JM and TM contributed equally.

    • Acknowledgements The authors are grateful to Professor Dr Rolf Graf (Department of Visceral and Transplantation Surgery, University Hospital, Zurich, Switzerland) and to Professor Dr Michael Bader (Max-Delbrück-Center for Molecular Medicine, Berlin, Germany) for providing us the TPH1−/− mice.

    • Contributors JM, TM and PP performed the fluorescence and fluid secretion measurements. AB, VV and ZR were involved in the study design and in the interpretation of the results. PH was the supervisor of the study and had full access to all results during this research project. The manuscript was drafted by PH.

    • Funding Our work was supported by the MTA-SZTE Momentum Grant (LP2014-10/2014) and the National Scientific Research Found grant K109756.

    • Competing interests None declared.

    • Provenance and peer review Not commissioned; internally peer reviewed.

    • Data sharing statement All results of the study have been included to the manuscript and no other persons, besides the authors, had access to the results.