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.
Highlights
Inflammation is part of the normal response of the host to invasion by harmful microorganisms or to tissue injury [1]
There is increasing evidence that poor and/or inappropriate resolution of inflammation participates in the pathogenesis of inflammatory bowel diseases (IBD) or asthma, being responsible in the long run for excessive tissue damage and pathology
There are a number of immune-mediated chronic diseases that might, at least in part, be controlled or prevented in an immune fit person, including IBD, allergy, and asthma developed in this review, as well as rheumatoid arthritis, chronic obstructive pulmonary disease (COPD), Parkinson’s disease, Alzheimer’s disease, multiple sclerosis, diabetes or myalgic encephalomyelitis
Summary
Inflammation is part of the normal response of the host to invasion by harmful microorganisms or to tissue injury [1]. Considered as a passive process, the natural resolution of acute inflammation is known as an active host response, with highly coordinated cellular and molecular events with release of anti-inflammatory cytokines, loss of receptors for proinflammatory signals, and production of a wide range of proresolving mediators including recently uncovered specialized pro-resolving lipid mediators (SPMs) that enable restoration of tissue homeostasis [3]. A failure in pro-resolving pathways may extend in time the actions of pro-inflammatory mechanisms resulting in prolonged or chronic inflammation with recurrent exacerbations, responsible in the long run for excessive tissue damage and pathology (Figure 1). Persistent airway inflammation in chronic lung diseases, such as asthma, may be due to defects in pro-resolving molecular pathways [5, 6]. We will discuss a series of interventions that can potentially promote resolution with a focus on “Th1/Th17 cell-driven” and “Th2 cell-driven” immune diseases, with IBD and asthma, as relevant examples
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