Bioactive Lipids and Chronic Inflammation: Managing the Fire Within

Abstract

Inflammation is an immune response that works as a contained fire that is pre-emptively sparked as a defensive process during infections or upon any kind of tissue insult, and that is spontaneously extinguished after elimination or termination of the damage. However, persistent and uncontrolled immune reactions act as a wildfire that promote chronic inflammation, unresolved tissue damage and, eventually, chronic diseases. A wide network of soluble mediators, among which endogenous bioactive lipids, governs all immune processes. They are secreted by basically all cells involved in inflammatory processes and constitute the crucial infrastructure that triggers, coordinates and confines inflammatory mechanisms. However, these molecules are also deeply involved in the detrimental transition from acute to chronic inflammation, be it for persistent or excessive action of pro-inflammatory lipids or for the impairment of the functions carried out by resolving ones. As a matter of fact, bioactive lipids have been linked, to date, to several chronic diseases, including rheumatoid arthritis, atherosclerosis, diabetes, cancer, inflammatory bowel disease, systemic lupus erythematosus, and multiple sclerosis. This review summarizes current knowledge on the involvement of the main classes of endogenous bioactive lipids—namely classical eicosanoids, pro-resolving lipid mediators, lysoglycerophospholipids/sphingolipids, and endocannabinoids—in the cellular and molecular mechanisms that lead to the pathogenesis of chronic disorders.

Bioactive lipids ALIAmides differentially modulate inflammatory responses of distinct subsets of primary human T lymphocytes

“…It is now widely accepted that numerous endogenous bioactive lipids control host defense and inflammation by building up a complex signaling network that modulates immune responses by differentially acting on distinct cellular effectors (26,27). In this scenario, ALIAmides have been reported to reduce pain (17) and to modulate acute and chronic inflammation mostly by acting on cells of innate immunity (18,28).…”

The Atlas of Inflammation-Resolution (AIR)

“…Acute inflammation is a highly coordinated, active, nonlinear spatial-temporal process for the removal of invading pathogens and the repair of damaged tissues to reestablish homeostasis [2][3][4] . If the acute inflammatory response is not resolved, it can contribute to organ pathology and amplify many widely occurring chronic inflammatory clinical phenotypes including arthritis, neurodegenerative diseases, metabolic syndrome, asthma, allergy, diabetes, aging, cancers, organ fibrosis, cardiovascular and periodontal diseases 5,6,15,[7][8][9][10][11][12][13][14] .…”

Impairment of DHA synthesis alters the expression of neuronal plasticity markers and the brain inflammatory status in mice

“…As already shown by our previous studies where impairment of systemic DHA synthesis affects specific immune cells, such as T-helper cells and macrophages 37,38 and given the important role of DHA in inflammatory responses, we next examined whether the deficient synthesis of this essential fatty acid can modulate the brain inflammatory status. For this purpose, we examined the expression of several markers F I G U R E 2 Synaptic plasticity markers expression is impaired in the cerebral cortex of KO mice.…”