Serine proteases as luminal mediators of intestinal barrier dysfunction and symptom severity in IBS.


Journal

Gut
ISSN: 1468-3288
Titre abrégé: Gut
Pays: England
ID NLM: 2985108R

Informations de publication

Date de publication:
01 2020
Historique:
received: 16 08 2018
revised: 13 03 2019
accepted: 16 03 2019
pubmed: 30 3 2019
medline: 18 12 2019
entrez: 30 3 2019
Statut: ppublish

Résumé

The intestinal lumen contains several proteases. Our aim was to determine the role of faecal proteases in mediating barrier dysfunction and symptoms in IBS. 39 patients with IBS and 25 healthy volunteers completed questionnaires, assessments of in vivo permeability, ex vivo colonic barrier function in Ussing chambers, tight junction (TJ) proteins, ultrastructural morphology and 16 s sequencing of faecal microbiota rRNA. A casein-based assay was used to measure proteolytic activity (PA) in faecal supernatants (FSNs). Colonic barrier function was determined in mice (ex-germ free) humanised with microbial communities associated with different human PA states. Patients with IBS had higher faecal PA than healthy volunteers. 8/20 postinfection IBS (PI-IBS) and 3/19 constipation- predominant IBS had high PA (>95th percentile). High-PA patients had more and looser bowel movements, greater symptom severity and higher in vivo and ex vivo colonic permeability. High-PA FSNs increased paracellular permeability, decreased occludin and increased phosphorylated myosin light chain (pMLC) expression. Serine but not cysteine protease inhibitor significantly blocked high-PA FSN effects on barrier. The effects on barrier were diminished by pharmacological or siRNA inhibition of protease activated receptor-2 (PAR-2). Patients with high-PA IBS had lower occludin expression, wider TJs on biopsies and reduced microbial diversity than patients with low PA. Mice humanised with high-PA IBS microbiota had greater in vivo permeability than those with low-PA microbiota. A subset of patients with IBS, especially in PI-IBS, has substantially high faecal PA, greater symptoms, impaired barrier and reduced microbial diversity. Commensal microbiota affects luminal PA that can influence host barrier function.

Identifiants

pubmed: 30923071
pii: gutjnl-2018-317416
doi: 10.1136/gutjnl-2018-317416
pmc: PMC6765451
mid: NIHMS1529240
doi:

Substances chimiques

Tight Junction Proteins 0
Serine Proteases EC 3.4.-

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

62-73

Subventions

Organisme : NIDDK NIH HHS
ID : K23 DK103911
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK084567
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK114007
Pays : United States
Organisme : NIDDK NIH HHS
ID : R03 DK120745
Pays : United States

Informations de copyright

© Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.

Déclaration de conflit d'intérêts

Competing interests: MG has served on the advisory board or received research support from Takeda, DongA, Ironwood and Napo.

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Auteurs

Shoko Edogawa (S)

Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.

Adam L Edwinson (AL)

Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.

Stephanie A Peters (SA)

Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.

Lakshmikanth L Chikkamenahalli (LL)

Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.

Wendy Sundt (W)

Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.

Sara Graves (S)

Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.

Sakteesh V Gurunathan (SV)

Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.

Margaret Breen-Lyles (M)

Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.

Stephen Johnson (S)

Division of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, Minnesota, USA.

Roy Dyer (R)

Immunochemical Core Laboratory, Mayo Clinic, Rochester, Minnesota, USA.

Rondell Graham (R)

Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA.

Jun Chen (J)

Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota, USA.

Purna Kashyap (P)

Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.

Gianrico Farrugia (G)

Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.

Madhusudan Grover (M)

Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.

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