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.
Highlights
Accumulating evidence shows indigenous gut microbes can interact with the human host through modulation of serotonin (5-HT) signaling
In doing so we demonstrate the ability of E. coli Nissle 1917 (EcN), but not a commensal E. coli strain (MG1655), to influence 5-HT signalling through interaction with, and modification of, secreted host derived factors
In order to assess the effect of EcN on 5-HT overflow from EC cells we first treated ex-vivo ileal tissue with cultures of EcN, or the gastrointestinal commensal E. coli MG1655 as a control, and measured extra-cellular levels of 5-HT post treatment
Summary
Accumulating evidence shows indigenous gut microbes can interact with the human host through modulation of serotonin (5-HT) signaling. 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. Measurement of 5-HT precursors and metabolites indicated EcN 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. The human gastro-intestinal (GI) tract harbours a dense and complex microbial community, which undertakes a range of functions beneficial to the human host[1,2,3,4,5] The pivotal role this gut microbiome is believed to play in human health has led to a growing interest in strategies to manipulate its structure and function, to treat or prevent a spectrum of GI disorders. As with other probiotics, the mechanisms through which EcN exerts these beneficial effects, and interact with the human host, remain largely undefined
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