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Listeria monocytogenes Inhibits Serotonin Transporter in Human Intestinal Caco-2 Cells
E Latorre1,2, A Pradilla3, B Chueca4,5
1Departamento Farmacología y Fisiología, Facultad de Veterinaria, Instituto de Investigación Sanitaria de Aragón (IIS), Universidad de Zaragoza, Zaragoza, Spain. e.latorre@exeter.ac.uk.
Microbial Ecology
|August 5, 2016
Summary
Living Listeria monocytogenes inhibits serotonin uptake by reducing the serotonin transporter (SERT) in intestinal cells. This bacterial effect, mediated by TLR10, may alter gut physiology and initiate inflammation.
Area of Science:
- Microbiology
- Gastroenterology
- Immunology
Background:
- Intestinal microorganisms influence gut physiology via immunological responses and modulation of the serotonergic system.
- Serotonin (5-HT), synthesized in the intestinal epithelium, regulates gut function.
- The serotonin transporter (SERT) in enterocytes controls intestinal 5-HT availability.
Purpose of the Study:
- To investigate the impact of Listeria monocytogenes infection on the intestinal serotonin transporter (SERT).
- To elucidate the mechanisms by which L. monocytogenes affects intestinal epithelial cells.
Main Methods:
- Utilized the Caco2/TC7 cell line as an in vitro model of enterocytes.
- Performed functional and molecular expression assays for SERT.
- Analyzed transcriptional changes in Toll-like receptors (TLR2 and TLR10).
Main Results:
- Living L. monocytogenes significantly inhibited serotonin uptake by reducing SERT expression at the brush border membrane.
- Inactivated bacteria and soluble metabolites did not affect SERT function or expression.
- L. monocytogenes induced transcriptional changes in TLR2 and TLR10, with TLR10 potentially mediating SERT inhibition.
Conclusions:
- L. monocytogenes directly inhibits intestinal SERT function and expression in an in vitro model.
- The observed effect is mediated by live bacteria and potentially involves TLR10 signaling.
- This mechanism may lead to increased intestinal serotonin availability, contributing to physiological changes and inflammation.
