Bacteria induce the release of proalgesic lipids by epithelial cells
(2019) Réseau Français de Recherche sur la Douleur — Location: Paris, France
Files
No attached file found for this publication.
Details
- Authors
- et. al.
- Abstract
- Irritable bowel syndrome (IBS) is characterized by visceral hypersensitivity associated with gut microbiota dysbiosis. Among the studied pronociceptive mediators, host and bacterial lipid compounds have been described as major regulators of visceral hypersensitivity. The aim of our study was to identify the role of the host and bacterial lipids interplay on visceral hypersensitivity. To differentiate bacterial and host lipids, bacteria were cultivated with 13C- glucose as unique source of carbon. 13C-labelled bacterial lipids were used to treat polarized epithelial cells. Quantification by mass spectrometry of 13C-labelled and unlabeled lipids in the basolateral compartment allowed us to determine epithelial and bacterial lipids potentially in contact with nerve endings. We quantified an increase of bacterial C10-3OH, C12AsnOH and C14AsnOH as well as epithelial 9,10-DiHOME and 12,13-DiHOME in the basolateral compartment. We assessed the ability of these lipids to increase intracellular calcium concentration in primary culture of mouse sensory neurons. Only the 9,10-DiHOME induced calcium flux in sensory neurons. This effect was inhibited by a pretreatment with a TRPV1 antagonist (AMG9810). Our study show that bacterial lipids induced the release of potentially proalgesic lipids by epithelial cells. Lipid metabolism could be the link between dysbiosis and visceral pain in IBS.
- Affiliations
Citations
Petitfils, C., & et al. (2019). Bacteria induce the release of proalgesic lipids by epithelial cells. Réseau Français de Recherche sur la Douleur, Paris, France.