Abstract
Leukotrienes (LTs) are lipid mediators that play pivotal roles in acute and chronic inflammation and allergic diseases. They exert their biological effects by binding to specific G-protein-coupled receptors. Each LT receptor subtype exhibits unique functions and expression patterns. LTs play roles in various allergic diseases, including asthma (neutrophilic asthma and aspirin-sensitive asthma), allergic rhinitis, atopic dermatitis, allergic conjunctivitis, and anaphylaxis. This review summarizes the biology of LTs and their receptors, recent developments in the area of anti-LT strategies (in settings such as ongoing clinical studies), and prospects for future therapeutic applications.
Highlights
Lipid mediators, which denote bioactive mediators derived from lipids, play roles in immune regulation, self-defense, and the maintenance of homeostasis in living systems
LT receptors BLT1 and BLT2 are activated by leukotriene B4 (LTB4), whereas CysLT1 and CysLT2 receptors are activated by cysteinyl LTs (CysLTs) [3]
LTs are involved in various inflammatory diseases, including asthma, allergic rhinitis (AR), atopic dermatitis (AD), allergic conjunctivitis, rheumatoid arthritis, anaphylaxis, chronic obstructive pulmonary disease (COPD), obliterative bronchiolitis after lung transplantation, and interstitial lung diseases [4]
Summary
Lipid mediators, which denote bioactive mediators derived from lipids, play roles in immune regulation, self-defense, and the maintenance of homeostasis in living systems They include prostaglandins (PGs) and leukotrienes (LTs), lysophospholipids (including sphingosine 1-phosphate), and endocannabinoids [1]. LTs, which are derived from arachidonic acid (5Z,8Z,11Z,14Z-eicosatetraenoic acid; AA) through two steps catalyzed by 5-lipoxygenase (5-LO), are inflammatory mediators that function in normal host defense and play roles in inflammatory diseases [2]. They exert their biological effects by binding to G-protein-coupled receptors (GPCRs).
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