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Dexamethasone induces ω3-derived immunoresolvents driving resolution of allergic airway inflammation.

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Chairakaki, Aikaterini-Dimitra 
Tamvakopoulos, Constantin 
Andreakos, Evangelos 


To the Editor: Resolution of inflammation has long been considered to be a passive process that ensues in an inflammatory response following the dilution of proinflammatory cues. However, this paradigm is shifting as it is becoming increasingly evident that resolution is an active reaction that uses a complex molecular machinery that orderly terminates inflammation. Among the multiple mechanisms involved, specialized proresolving lipid mediators (SPMs) such as resolvins, protectins, and lipoxins have taken center stage.1 These are derived from ω3 and ω6 polyunsaturated fatty acids through complex intracellular and transcellular biosynthetic pathways, and promote resolution of inflammation by their manifold and concerted functions inhibiting leukocyte trafficking, dampening proinflammatory signaling, inducing apoptosis, and promoting anti-inflammatory M2-like macrophage phenotypes, efferocytosis, and tissue restitution.1



Animals, Anti-Inflammatory Agents, Arachidonate 12-Lipoxygenase, Arachidonate 15-Lipoxygenase, Asthma, Dexamethasone, Dinoprostone, Disease Models, Animal, Fatty Acids, Omega-3, Humans, Hypersensitivity, Inflammation, Mice, Mice, Inbred C57BL, Mice, Knockout, Prostaglandin D2, Respiratory Hypersensitivity

Journal Title

Journal of Allergy and Clinical Immunology

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Mosby Inc.
This work was supported by core funding from the Hellenic Ministry of Education, Research and Religious Affairs and the Hellenic Ministry of Health, and by the research grants PREDICTA (contract no. 260895) from the European Commission, MIDAS (contract no. MIS 377047), and RESOLVE-ASTHMA (contract no. 2601) from the Hellenic Ministry of Education, Research and Religious Affairs.