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Dietary lipids fuel GPX4-restricted enteritis resembling Crohn's disease.

Accepted version
Peer-reviewed

Type

Article

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Authors

Mayr, Lisa 
Grabherr, Felix 
Schwärzler, Julian 
Reitmeier, Isabelle 

Abstract

The increased incidence of inflammatory bowel disease (IBD) has become a global phenomenon that could be related to adoption of a Western life-style. Westernization of dietary habits is partly characterized by enrichment with the ω-6 polyunsaturated fatty acid (PUFA) arachidonic acid (AA), which entails risk for developing IBD. Glutathione peroxidase 4 (GPX4) protects against lipid peroxidation (LPO) and cell death termed ferroptosis. We report that small intestinal epithelial cells (IECs) in Crohn's disease (CD) exhibit impaired GPX4 activity and signs of LPO. PUFAs and specifically AA trigger a cytokine response of IECs which is restricted by GPX4. While GPX4 does not control AA metabolism, cytokine production is governed by similar mechanisms as ferroptosis. A PUFA-enriched Western diet triggers focal granuloma-like neutrophilic enteritis in mice that lack one allele of Gpx4 in IECs. Our study identifies dietary PUFAs as a trigger of GPX4-restricted mucosal inflammation phenocopying aspects of human CD.

Description

Keywords

Adult, Animals, Cell Death, Crohn Disease, Dietary Fats, Enteritis, Fatty Acids, Unsaturated, Female, Glutathione Peroxidase, Humans, Inflammation, Lipid Peroxidation, Male, Mice, Mice, Inbred C57BL, Middle Aged, Phospholipid Hydroperoxide Glutathione Peroxidase

Journal Title

Nat Commun

Conference Name

Journal ISSN

2041-1723
2041-1723

Volume Title

11

Publisher

Springer Science and Business Media LLC

Rights

All rights reserved