Chromogranin A regulates gut permeability via the antagonistic actions of its proteolytic peptides.

Catestatin chromogranin A enteroendocrine cells epithelial tight junctions gut barrier inflammatory bowel disease

Journal

Acta physiologica (Oxford, England)
ISSN: 1748-1716
Titre abrégé: Acta Physiol (Oxf)
Pays: England
ID NLM: 101262545

Informations de publication

Date de publication:
06 2021
Historique:
revised: 23 03 2021
received: 30 11 2020
accepted: 25 03 2021
pubmed: 31 3 2021
medline: 19 8 2021
entrez: 30 3 2021
Statut: ppublish

Résumé

A "leaky" gut barrier has been implicated in the initiation and progression of a multitude of diseases, for example, inflammatory bowel disease (IBD), irritable bowel syndrome and celiac disease. Here we show how pro-hormone Chromogranin A (CgA), produced by the enteroendocrine cells, and Catestatin (CST: hCgA Colon tissues from region-specific CST-knockout (CST-KO) mice, CgA-knockout (CgA-KO) and WT mice were analysed by immunohistochemistry, western blot, ultrastructural and flowcytometry studies. FITC-dextran assays were used to measure intestinal barrier function. Mice were supplemented with CST or CgA fragment pancreastatin (PST: CgA Plasma levels of CST were elevated in IBD patients. CST-KO mice displayed (a) elongated tight, adherens junctions and desmosomes similar to IBD patients, (b) elevated expression of Claudin 2, and (c) gut inflammation. Plasma FITC-dextran measurements showed increased intestinal paracellular permeability in the CST-KO mice. This correlated with a higher ratio of Firmicutes to Bacteroidetes, a dysbiotic pattern commonly encountered in various diseases. Supplementation of CST-KO mice with recombinant CST restored paracellular permeability and reversed inflammation, whereas CgA-KO mice supplementation with CST and/or PST in CgA-KO mice showed that intestinal paracellular permeability is regulated by the antagonistic roles of these two peptides: CST reduces and PST increases permeability. The pro-hormone CgA regulates the intestinal paracellular permeability. CST is both necessary and sufficient to reduce permeability and primarily acts by antagonizing PST.

Identifiants

pubmed: 33783968
doi: 10.1111/apha.13655
pmc: PMC8341099
mid: NIHMS1724254
doi:

Substances chimiques

Chromogranin A 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

e13655

Subventions

Organisme : BLRD VA
ID : I01 BX003934
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI141630
Pays : United States

Informations de copyright

© 2021 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.

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Auteurs

Elke M Muntjewerff (EM)

Department of Tumor Immunology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, the Netherlands.

Kechun Tang (K)

VA San Diego Healthcare System, San Diego, CA, USA.

Lisanne Lutter (L)

Center for Translational Immunology, Utrecht University Medical Center, Utrecht, the Netherlands.
Department of Gastroenterology and Hepatology, Utrecht University Medical Center, Utrecht, the Netherlands.

Gustaf Christoffersson (G)

Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
Department of Medical Cell biology, Uppsala University, Uppsala, Sweden.

Mara J T Nicolasen (MJT)

Department of Tumor Immunology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, the Netherlands.

Hong Gao (H)

Department of Medicine, University of California San Diego, La Jolla, CA, USA.

Gajanan D Katkar (GD)

Department of Cellular and Molecular Medicine, University of California San Diego, La Jolla, CA, USA.

Soumita Das (S)

Department of Pathology, University of California San Diego, La Jolla, CA, USA.

Martin Ter Beest (M)

Department of Tumor Immunology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, the Netherlands.

Wei Ying (W)

Department of Medicine, University of California San Diego, La Jolla, CA, USA.

Pradipta Ghosh (P)

Department of Medicine, University of California San Diego, La Jolla, CA, USA.
Department of Cellular and Molecular Medicine, University of California San Diego, La Jolla, CA, USA.

Sahar El Aidy (S)

Department of Molecular Immunology and Microbiology, Groningen Biomolecular Sciences and Biotechnology Institute, University of Groningen, Groningen, the Netherlands.

Bas Oldenburg (B)

Department of Gastroenterology and Hepatology, Utrecht University Medical Center, Utrecht, the Netherlands.

Geert van den Bogaart (G)

Department of Tumor Immunology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, the Netherlands.
Department of Molecular Immunology and Microbiology, Groningen Biomolecular Sciences and Biotechnology Institute, University of Groningen, Groningen, the Netherlands.

Sushil K Mahata (SK)

VA San Diego Healthcare System, San Diego, CA, USA.
Department of Medicine, University of California San Diego, La Jolla, CA, USA.

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Classifications MeSH