Eicosanoid Mediators in the Airway Inflammation of Asthmatic Patients: What is New?.
10.4168/aair.2016.8.6.481
- Author:
Marek SANAK
1
Author Information
1. Department of Internal Medicine, Jagiellonian University Medical College, Krakow, Poland. nfsanak@cyf-kr.edu.pl
- Publication Type:Review
- Keywords:
Eicosanoids;
asthma;
aspirin exacerbated respiratory disease
- MeSH:
Arachidonic Acid;
Asthma;
Eicosanoids;
Eosinophils;
Granulocytes;
Humans;
Hypersensitivity;
Immunoassay;
Inflammation*;
Isoprostanes;
Leukotrienes;
Macrophages;
Oxygen;
Phenotype;
Spectrum Analysis;
Sputum
- From:Allergy, Asthma & Immunology Research
2016;8(6):481-490
- CountryRepublic of Korea
- Language:English
-
Abstract:
Lipid mediators contribute to inflammation providing both pro-inflammatory signals and terminating the inflammatory process by activation of macrophages. Among the most significant biologically lipid mediators, these are produced by free-radical or enzymatic oxygenation of arachidonic acid named "eicosanoids". There were some novel eicosanoids identified within the last decade, and many of them are measurable in clinical samples by affordable chromatography-mass spectrometry equipment or sensitive immunoassays. In this review, we present some recent advances in understanding of the signaling by eicosanoid mediators during asthmatic airway inflammation. Eicosanoid profiling in the exhaled breath condensate, induced sputum, or their metabolites measurements in urine is complementary to the cellular phenotyping of asthmatic inflammation. Special attention is paid to aspirin-exacerbated respiratory disease, a phenotype of asthma manifested by the most profound changes in the profile of eicosanoids produced. A hallmark of this type of asthma with hypersensitivity to non-steroid anti-inflammatory drugs (NSAIDs) is to increase biosynthesis of cysteinyl leukotrienes on the systemic level. It depends on transcellular biosynthesis of leukotriene C₄ by platelets that adhere to granulocytes releasing leukotriene A₄. However, other abnormalities are also reported in this type of asthma as a resistance to anti-inflammatory activity of prostaglandin E₂ or a robust eosinophil interferon-γ response resulting in cysteinyl leukotrienes production. A novel mechanism is also discussed in which an isoprostane structurally related to prostaglandin E₂ is released into exhaled breath condensate during a provoked asthmatic attack. However, it is concluded that any single eicosanoid or even their complex profile can hardly provide a thorough explanation for the mechanism of asthmatic inflammation.
