Barnig C^1,2, Bezema T³, Calder PC^4,5, Charloux A^1,2, Frossard N⁶, Garssen J^7,8, Haworth O⁹, Dilevskaya K¹⁰, Levi-Schaffer F¹¹, Lonsdorfer E^1,2, Wauben M¹², Kraneveld AD^7,13, Te Velde AA¹⁴. Front Immunol. 2019 Jul 23;10:1699. doi: 10.3389/fimmu.2019.01699. eCollection 2019.

Author information

1 Department of Chest Disease, Strasbourg University Hospital, Strasbourg, France.

2 Equipe d'accueil 3072, University of Strasbourg, Strasbourg, France.

3 Immunowell Foundation, Utrecht, Netherlands.

4 Human Development and Health, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.

5 National Institute for Health Research Southampton Biomedical Research Centre, University Hospital Southampton NHS Foundation Trust and University of Southampton, Southampton, United Kingdom.

6 UMR 7200 CNRS/Université de Strasbourg, Laboratoire d'Innovation Thérapeutique and LabEx MEDALIS, Faculté de Pharmacie, Strasbourg, France.

7 Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, Netherlands.

8 Nutricia Research, Utrecht, Netherlands.

9 Biochemical Pharmacology, William Harvey Research Institute, Bart's School of Medicine and Queen Mary University of London, London, United Kingdom.

10 Division of Pharmacology, Faculty of Science, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Utrecht, Netherlands.

11 Pharmacology and Experimental Therapeutics Unit, Faculty of Medicine, School of Pharmacy, Institute for Drug Research, The Hebrew University of Jerusalem, Jerusalem, Israel.

12 Department of Biochemistry & Cell Biology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, Netherlands.

13 Institute for Risk Assessment Sciences, Faculty of Veterinary Medicine, Utrecht University, Utrecht, Netherlands.

14 Amsterdam UMC, Tytgat Institute for Liver and Intestinal Research, University of Amsterdam, AGEM, Amsterdam, Netherlands.

Abstract

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 (IBD) 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.