Proton pump inhibitors enhance intestinal permeability via dysbiosis of gut microbiota under stressed conditions in mice.


Journal

Neurogastroenterology and motility
ISSN: 1365-2982
Titre abrégé: Neurogastroenterol Motil
Pays: England
ID NLM: 9432572

Informations de publication

Date de publication:
07 2020
Historique:
received: 28 10 2019
revised: 27 02 2020
accepted: 02 03 2020
pubmed: 23 4 2020
medline: 16 7 2021
entrez: 23 4 2020
Statut: ppublish

Résumé

Intestinal permeability and psychological stress are considered the key mechanism(s) in functional dyspepsia (FD). Although proton pump inhibitors (PPIs) are commonly used for the treatment of FD, the effect of PPIs on intestinal permeability has not been elucidated. This study investigated the effect of PPI on intestinal permeability under stressed conditions. C57BL/6J mice were subjected to water avoidance stress (WAS) and administered rabeprazole (40 mg/kg) or vehicle treatment (VT). We then evaluated intestinal permeability both in vivo and ex vivo using plasma fluorescein isothiocyanate-dextran and by assessing the paracellular permeability and transepithelial electrical resistance (TEER) in an Ussing chamber, respectively. Furthermore, we evaluated the effect of PPI-treated fecal microbiota transplant (FMT) on intestinal permeability in vivo. Microbiota profiles of donor feces were assessed by 16S rRNA gene analysis using MiSeq and QIIME2. In the WAS treatment, PPI significantly enhanced intestinal permeability in vivo compared to that in VT. Moreover, PPI significantly increased paracellular permeability and decreased TEER in the duodenum and jejunum, respectively, compared to those in VT under stressed conditions. Moreover, both vasoactive intestinal peptide (VIP) receptor antagonist and ketotifen significantly reversed the effect of PPI on intestinal permeability. Furthermore, PPI-treated FMT significantly increased the intestinal permeability in vivo compared to that in vehicle-treated FMT. Proton pump inhibitors treatment altered the gut microbiota composition, indicating that PPI induced dysbiosis. Under stressed conditions, PPI enhances intestinal permeability via dysbiosis of gut microbiota. Vasoactive intestinal peptide and mast cells are also implicated in the underlying mechanisms.

Sections du résumé

BACKGROUND
Intestinal permeability and psychological stress are considered the key mechanism(s) in functional dyspepsia (FD). Although proton pump inhibitors (PPIs) are commonly used for the treatment of FD, the effect of PPIs on intestinal permeability has not been elucidated. This study investigated the effect of PPI on intestinal permeability under stressed conditions.
METHODS
C57BL/6J mice were subjected to water avoidance stress (WAS) and administered rabeprazole (40 mg/kg) or vehicle treatment (VT). We then evaluated intestinal permeability both in vivo and ex vivo using plasma fluorescein isothiocyanate-dextran and by assessing the paracellular permeability and transepithelial electrical resistance (TEER) in an Ussing chamber, respectively. Furthermore, we evaluated the effect of PPI-treated fecal microbiota transplant (FMT) on intestinal permeability in vivo. Microbiota profiles of donor feces were assessed by 16S rRNA gene analysis using MiSeq and QIIME2.
KEY RESULTS
In the WAS treatment, PPI significantly enhanced intestinal permeability in vivo compared to that in VT. Moreover, PPI significantly increased paracellular permeability and decreased TEER in the duodenum and jejunum, respectively, compared to those in VT under stressed conditions. Moreover, both vasoactive intestinal peptide (VIP) receptor antagonist and ketotifen significantly reversed the effect of PPI on intestinal permeability. Furthermore, PPI-treated FMT significantly increased the intestinal permeability in vivo compared to that in vehicle-treated FMT. Proton pump inhibitors treatment altered the gut microbiota composition, indicating that PPI induced dysbiosis.
CONCLUSIONS AND INFERENCES
Under stressed conditions, PPI enhances intestinal permeability via dysbiosis of gut microbiota. Vasoactive intestinal peptide and mast cells are also implicated in the underlying mechanisms.

Identifiants

pubmed: 32319196
doi: 10.1111/nmo.13841
doi:

Substances chimiques

Proton Pump Inhibitors 0
Rabeprazole 32828355LL
Corticosterone W980KJ009P

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

e13841

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

© 2020 John Wiley & Sons Ltd.

Références

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Auteurs

Shingo Takashima (S)

Department of Gastroenterology, Osaka City University Graduate School of Medicine, Osaka, Japan.

Fumio Tanaka (F)

Department of Gastroenterology, Osaka City University Graduate School of Medicine, Osaka, Japan.

Yunosuke Kawaguchi (Y)

Department of Immunology and Genomics, Osaka City University Graduate School of Medicine, Osaka, Japan.

Yuki Usui (Y)

Division of Systems Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Kosuke Fujimoto (K)

Department of Immunology and Genomics, Osaka City University Graduate School of Medicine, Osaka, Japan.
Division of Innate Immune Regulation, International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Yuji Nadatani (Y)

Department of Gastroenterology, Osaka City University Graduate School of Medicine, Osaka, Japan.

Koji Otani (K)

Department of Gastroenterology, Osaka City University Graduate School of Medicine, Osaka, Japan.

Shuhei Hosomi (S)

Department of Gastroenterology, Osaka City University Graduate School of Medicine, Osaka, Japan.

Yasuaki Nagami (Y)

Department of Gastroenterology, Osaka City University Graduate School of Medicine, Osaka, Japan.

Noriko Kamata (N)

Department of Gastroenterology, Osaka City University Graduate School of Medicine, Osaka, Japan.

Koichi Taira (K)

Department of Gastroenterology, Osaka City University Graduate School of Medicine, Osaka, Japan.

Tetsuya Tanigawa (T)

Department of Gastroenterology, Osaka City University Graduate School of Medicine, Osaka, Japan.

Toshio Watanabe (T)

Department of Gastroenterology, Osaka City University Graduate School of Medicine, Osaka, Japan.

Seiya Imoto (S)

Division of Health Medical Data Science, Health Intelligence Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Satoshi Uematsu (S)

Department of Immunology and Genomics, Osaka City University Graduate School of Medicine, Osaka, Japan.
Division of Innate Immune Regulation, International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Yasuhiro Fujiwara (Y)

Department of Gastroenterology, Osaka City University Graduate School of Medicine, Osaka, Japan.

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