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Nat Commun. 2017 Nov 3;8(1):1314. doi: 10.1038/s41467-017-01403-9.

Identification of an analgesic lipopeptide produced by the probiotic Escherichia coli strain Nissle 1917.

Author information

1
IRSD, Université de Toulouse, INSERM, INRA, INP-ENVT, Université de Toulouse 3 Paul Sabatier, 31024, Toulouse, France.
2
CHU Toulouse, Hôpital Purpan, Service de bactériologie-hygiène, 31024, Toulouse, France.
3
MetaToulLipidomics Facility, INSERM UMR1048, 31432, Toulouse, France.
4
Institut des Biomolécules Max Mousseron IBMM, UMR 5247 CNRS, Université de Montpellier-ENSCM, 34093, Montpellier, France.
5
Sorbonne Université, UPMC Univ Paris 06, CNRS, Institut Parisien de Chimie Moléculaire (IPCM), 75005, Paris, France.
6
LISBP, Université de Toulouse, CNRS, INRA, INSA, 31077, Toulouse, France.
7
IRSD, Université de Toulouse, INSERM, INRA, INP-ENVT, Université de Toulouse 3 Paul Sabatier, 31024, Toulouse, France. nicolas.cenac@inserm.fr.

Abstract

Administration of the probiotic Escherichia coli strain Nissle 1917 (EcN) decreases visceral pain associated with irritable bowel syndrome. Mutation of clbA, a gene involved in the biosynthesis of secondary metabolites, including colibactin, was previously shown to abrogate EcN probiotic activity. Here, we show that EcN, but not an isogenic clbA mutant, produces an analgesic lipopeptide. We characterize lipoamino acids and lipopeptides produced by EcN but not by the mutant by online liquid chromatography mass spectrometry. One of these lipopeptides, C12AsnGABAOH, is able to cross the epithelial barrier and to inhibit calcium flux induced by nociceptor activation in sensory neurons via the GABAB receptor. C12AsnGABAOH inhibits visceral hypersensitivity induced by nociceptor activation in mice. Thus, EcN produces a visceral analgesic, which could be the basis for the development of new visceral pain therapies.

PMID:
29101366
PMCID:
PMC5670229
DOI:
10.1038/s41467-017-01403-9
[Indexed for MEDLINE]
Free PMC Article

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