Fecal dysbiosis associated with colonic hypersensitivity and behavioral alterations in chronically Blastocystis-infected rats.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
04 06 2020
Historique:
received: 22 10 2019
accepted: 11 04 2020
entrez: 6 6 2020
pubmed: 6 6 2020
medline: 15 12 2020
Statut: epublish

Résumé

Infectious gastroenteritis is a risk factor for the development of post-infectious Irritable Bowel Syndrome (PI-IBS). Recent clinical studies reported a higher prevalence of the intestinal parasite Blastocystis in IBS patients. Using a rat model, we investigated the possible association between Blastocystis infection, colonic hypersensitivity (CHS), behavioral disturbances and gut microbiota changes. Rats were orally infected with Blastocystis subtype 4 (ST4) cysts, isolated from human stool samples. Colonic sensitivity was assessed by colorectal distension and animal behavior with an automatic behavior recognition system (PhenoTyper), the Elevated Plus Maze test and the Forced Swimming tests. Feces were collected at different time points after infection to study microbiota composition by 16 S rRNA amplicon sequencing and for short-chain fatty acid (SFCA) analysis. Blastocystis-infected animals had non-inflammatory CHS with increased serine protease activity. Infection was also associated with anxiety- and depressive-like behaviors. Analysis of fecal microbiota composition showed an increase in bacterial richness associated with altered microbiota composition. These changes included an increase in the relative abundance of Oscillospira and a decrease in Clostridium, which seem to be associated with lower levels of SCFAs in the feces from infected rats. Our findings suggest that experimental infection of rats with Blastocystis mimics IBS symptoms with the establishment of CHS related to microbiota and metabolic shifts.

Sections du résumé

BACKGROUND
Infectious gastroenteritis is a risk factor for the development of post-infectious Irritable Bowel Syndrome (PI-IBS). Recent clinical studies reported a higher prevalence of the intestinal parasite Blastocystis in IBS patients. Using a rat model, we investigated the possible association between Blastocystis infection, colonic hypersensitivity (CHS), behavioral disturbances and gut microbiota changes.
METHODS
Rats were orally infected with Blastocystis subtype 4 (ST4) cysts, isolated from human stool samples. Colonic sensitivity was assessed by colorectal distension and animal behavior with an automatic behavior recognition system (PhenoTyper), the Elevated Plus Maze test and the Forced Swimming tests. Feces were collected at different time points after infection to study microbiota composition by 16 S rRNA amplicon sequencing and for short-chain fatty acid (SFCA) analysis.
RESULTS
Blastocystis-infected animals had non-inflammatory CHS with increased serine protease activity. Infection was also associated with anxiety- and depressive-like behaviors. Analysis of fecal microbiota composition showed an increase in bacterial richness associated with altered microbiota composition. These changes included an increase in the relative abundance of Oscillospira and a decrease in Clostridium, which seem to be associated with lower levels of SCFAs in the feces from infected rats.
CONCLUSIONS
Our findings suggest that experimental infection of rats with Blastocystis mimics IBS symptoms with the establishment of CHS related to microbiota and metabolic shifts.

Identifiants

pubmed: 32499543
doi: 10.1038/s41598-020-66156-w
pii: 10.1038/s41598-020-66156-w
pmc: PMC7272397
doi:

Substances chimiques

Fatty Acids, Volatile 0
Serine Proteases EC 3.4.-

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

9146

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Auteurs

Manon Defaye (M)

Université Clermont Auvergne, 3iHP, CNRS, Laboratoire Microorganismes: Génome et Environnement, F-63000, Clermont-Ferrand, France.
Université Clermont Auvergne, 3iHP, Inserm U1107, NeuroDol, Clermont-Ferrand, France.

Céline Nourrisson (C)

Université Clermont Auvergne, 3iHP, CNRS, Laboratoire Microorganismes: Génome et Environnement, F-63000, Clermont-Ferrand, France.
Université Clermont Auvergne, CHU, 3iHP, CNRS, Laboratoire Microorganismes: Génome et Environnement, F-63000, Clermont-Ferrand, France.

Elodie Baudu (E)

Université Clermont Auvergne, 3iHP, Inserm U1107, NeuroDol, Clermont-Ferrand, France.
Université Clermont Auvergne, 3iHP, Inserm U1071, USC INRA 2018, Microbes, Intestin, Inflammation et Susceptibilité de l'Hôte, Clermont-Ferrand, France.

Amandine Lashermes (A)

Université Clermont Auvergne, 3iHP, Inserm U1107, NeuroDol, Clermont-Ferrand, France.

Maëva Meynier (M)

Université Clermont Auvergne, 3iHP, Inserm U1107, NeuroDol, Clermont-Ferrand, France.

Mathieu Meleine (M)

Université Clermont Auvergne, 3iHP, Inserm U1107, NeuroDol, Clermont-Ferrand, France.

Ivan Wawrzyniak (I)

Université Clermont Auvergne, 3iHP, CNRS, Laboratoire Microorganismes: Génome et Environnement, F-63000, Clermont-Ferrand, France.

Virginie Bonnin (V)

Université Clermont Auvergne, 3iHP, Inserm U1071, USC INRA 2018, Microbes, Intestin, Inflammation et Susceptibilité de l'Hôte, Clermont-Ferrand, France.

Julie Barbier (J)

Université Clermont Auvergne, 3iHP, Inserm U1107, NeuroDol, Clermont-Ferrand, France.

Benoit Chassaing (B)

Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA.
Neuroscience Institute, Georgia State University, Atlanta, GA, USA.
INSERM, U1016, team "Mucosal microbiota in chronic inflammatory diseases", Paris, France.
Université de Paris, Paris, France.

Catherine Godfraind (C)

CHU Clermont-Ferrand, Service d'Anatomopathologie, 63003, Clermont-Ferrand, France.

Agathe Gelot (A)

Université Clermont Auvergne, 3iHP, Inserm U1107, NeuroDol, Clermont-Ferrand, France.

Nicolas Barnich (N)

Université Clermont Auvergne, 3iHP, Inserm U1071, USC INRA 2018, Microbes, Intestin, Inflammation et Susceptibilité de l'Hôte, Clermont-Ferrand, France.

Denis Ardid (D)

Université Clermont Auvergne, 3iHP, Inserm U1107, NeuroDol, Clermont-Ferrand, France.

Mathilde Bonnet (M)

Université Clermont Auvergne, 3iHP, Inserm U1071, USC INRA 2018, Microbes, Intestin, Inflammation et Susceptibilité de l'Hôte, Clermont-Ferrand, France.

Frédéric Delbac (F)

Université Clermont Auvergne, 3iHP, CNRS, Laboratoire Microorganismes: Génome et Environnement, F-63000, Clermont-Ferrand, France.

Frédéric Antonio Carvalho (FA)

Université Clermont Auvergne, 3iHP, Inserm U1107, NeuroDol, Clermont-Ferrand, France. frederic.carvalho@uca.fr.

Philippe Poirier (P)

Université Clermont Auvergne, 3iHP, CNRS, Laboratoire Microorganismes: Génome et Environnement, F-63000, Clermont-Ferrand, France. ppoirier@chu-clermontferrand.fr.
Université Clermont Auvergne, CHU, 3iHP, CNRS, Laboratoire Microorganismes: Génome et Environnement, F-63000, Clermont-Ferrand, France. ppoirier@chu-clermontferrand.fr.

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