Nature Communications (Jan 2022)
Oxylipin metabolism is controlled by mitochondrial β-oxidation during bacterial inflammation
- Mariya Misheva,
- Konstantinos Kotzamanis,
- Luke C. Davies,
- Victoria J. Tyrrell,
- Patricia R. S. Rodrigues,
- Gloria A. Benavides,
- Christine Hinz,
- Robert C. Murphy,
- Paul Kennedy,
- Philip R. Taylor,
- Marcela Rosas,
- Simon A. Jones,
- James E. McLaren,
- Sumukh Deshpande,
- Robert Andrews,
- Nils Helge Schebb,
- Magdalena A. Czubala,
- Mark Gurney,
- Maceler Aldrovandi,
- Sven W. Meckelmann,
- Peter Ghazal,
- Victor Darley-Usmar,
- Daniel A. White,
- Valerie B. O’Donnell
Affiliations
- Mariya Misheva
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- Konstantinos Kotzamanis
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- Luke C. Davies
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- Victoria J. Tyrrell
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- Patricia R. S. Rodrigues
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- Gloria A. Benavides
- Department of Pathology, University of Alabama at Birmingham
- Christine Hinz
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- Robert C. Murphy
- Department of Pharmacology, University of Colorado Denver
- Paul Kennedy
- Cayman Chemical
- Philip R. Taylor
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- Marcela Rosas
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- Simon A. Jones
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- James E. McLaren
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- Sumukh Deshpande
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- Robert Andrews
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- Nils Helge Schebb
- Chair of Food Chemistry, Faculty of Mathematics and Natural Sciences, University of Wuppertal
- Magdalena A. Czubala
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- Mark Gurney
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- Maceler Aldrovandi
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- Sven W. Meckelmann
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- Peter Ghazal
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- Victor Darley-Usmar
- Department of Pathology, University of Alabama at Birmingham
- Daniel A. White
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- Valerie B. O’Donnell
- Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University
- DOI
- https://doi.org/10.1038/s41467-021-27766-8
- Journal volume & issue
-
Vol. 13,
no. 1
pp. 1 – 20
Abstract
Oxylipins are lipid mediators generated during infection for regulating inflammatory responses, but how they are removed is not completely clear. Here the authors show that cellular oxylipin removal is linked to mitochondria β-oxidation by CPT1, a mitochondria lipid importer protein, to serve as a metabolic checkpoint for oxylipin homeostasis and inflammation.
