Escherichia coli Nissle 1917 enhances bioavailability of serotonin in gut tissues through modulation of synthesis and clearance

Jonathan Nzakizwanayo, Cinzia Dedi, Guy Standen, Wendy M Macfarlane, Bhavik A Patel, Brian V Jones

Research output: Contribution to journalArticlepeer-review

39 Citations (Scopus)

Abstract

Accumulating evidence shows indigenous gut microbes can interact with the human host through modulation of serotonin (5-HT) signaling. Here we investigate the impact of the probiotic Escherichia coli Nissle 1917 (EcN) on 5-HT signalling in gut tissues. Ex-vivo mouse ileal tissue sections were treated with either EcN or the human gut commensal MG1655, and effects on levels of 5-HT, precursors, and metabolites, were evaluated using amperometry and high performance liquid chromatography with electrochemical detection (HPLC-EC). Exposure of tissue to EcN cells, but not MG1655 cells, was found to increase levels of extra-cellular 5-HT. These effects were not observed when tissues were treated with cell-free supernatant from bacterial cultures. In contrast, when supernatant recovered from untreated ileal tissue was pre-incubated with EcN, the derivative cell-free supernatant was able to elevate 5-HT overflow when used to treat fresh ileal tissue. Measurement of 5-HT precursors and metabolites indicated EcN also increases intracellular 5-HTP and reduces 5-HIAA. The former pointed to modulation of tryptophan hydroxylase-1 to enhance 5-HT synthesis, while the latter indicates an impact on clearance into enterocytes through SERT. Taken together, these findings show EcN is able to enhance 5-HT bioavailability in ileal tissues through interaction with compounds secreted from host tissues.

Original languageEnglish
Article number17324
Number of pages13
JournalScientific Reports
Volume5
DOIs
Publication statusPublished - 30 Nov 2015

Keywords

  • Animals
  • Biological Availability
  • Escherichia coli/physiology
  • Extracellular Space/metabolism
  • Fatty Acids/metabolism
  • Gastrointestinal Tract/metabolism
  • Male
  • Mice
  • Models, Biological
  • Serotonin/metabolism
  • Synaptic Transmission

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