Activation of resolution pathways to prevent and fight chronic inflammation
- 1Université de Strasbourg, France
- 2Immunowell Foundation, Netherlands
- 3University Hospital Southampton NHS Foundation Trust, United Kingdom
- 4Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Netherlands
- 5William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, United Kingdom
- 6Utrecht University, Netherlands
- 7Hebrew University of Jerusalem, Israel
- 8University Medical Center Amsterdam, Netherlands
Formerly considered as a passive process, the resolution of acute inflammation is now recognized as an active host response, with a cascade of coordinated cellular and molecular events, that promotes termination of the inflammatory response and initiates tissue repair and healing. In a state of immune fitness, the resolution of inflammation is contained in time and space enabling the restoration of tissue homeostasis.
There is increasing evidence that poor and/or inappropriate resolution of inflammation participates in the pathogenesis of chronic inflammatory diseases, extending in time the actions of pro-inflammatory mechanisms, and responsible in the long run for excessive tissue damage and pathology.
In this review, we will focus on how resolution can be the target for therapy in ‘Th1/Th17 cell-driven’ immune diseases and ‘Th2 cell-driven’ immune diseases, with inflammatory bowel diseases and asthma, as relevant examples.
We describe the main cells and mediators stimulating the resolution of inflammation and discuss how pharmacological and dietary interventions but also life style factors, physical and psychological conditions, might influence the resolution phase.
A better understanding of the impact of endogenous and exogenous factors on the resolution of inflammation might open a whole area in the development of personalized therapies in non-resolving chronic inflammatory diseases.
Keywords: Resolution, Inflammation, immune fitness , Eicosanoids, Asthma, Chronic inflammatory bowel disease
Received: 06 Nov 2018;
Accepted: 08 Jul 2019.
Edited by:Fulvio D'Acquisto, Department of Life Sciences, University of Roehampton, United Kingdom
Reviewed by:Francesco Annunziato, University of Florence, Italy
Valerio Chiurchiù, Campus Bio-Medico University, Italy
Lorenzo Cosmi, University of Florence, Italy
Copyright: © 2019 Barnig, Bezema, Calder, Charloux, Frossard, Garssen, Haworth, Dilevskaya, Levi-Schaffer, Lonsdorfer, Wauben, Kraneveld and Te Velde. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Dr. Cindy Barnig, Université de Strasbourg, Strasbourg, 67081 CEDEX, Alsace, France, firstname.lastname@example.org