A turn on and a turn off: BLT1 and BLT2 mechanisms in the lung. (August 2014)

• Record Type: Journal Article
• Authors: Watanabe, Masaki; Machida, Kentaro; Inoue, Hiromasa
• Is Part Of: Expert review of respiratory medicine. Volume 8:Number 4(2014)
• Page Start: 381
• Page End: 383
• Publication Date: 2014-08
• Subjects: Respiratory organs -- Diseases -- Periodicals; Respiratory organs -- Diseases -- Treatment -- Periodicals; 616.2005
• DOI: 10.1586/17476348.2014.908715
• Languages: English
• ISSNs: 1747-6348

Abstract

<abstract> <title> <x xml:space="preserve">Abstract</x> </title> <p>Leukotriene B₄ (LTB₄), a potent lipid mediator of inflammation derived from arachidonic acid through the action of 5-lipoxygenase, has been implicated in the pathophysiology of several inflammatory diseases, including asthma and chronic obstructive pulmonary disease. A high-affinity LTB₄ receptor BLT1 has been shown to exert proinflammatory roles. A cyclooxygenase metabolite, 12(S)-hydroxyheptadeca-5Z, 8E, 10E-trienoic acid (12-HHT), is an endogenous ligand for BLT2, a low-affinity LTB₄ receptor. The recent study indicated that BLT2 has a protective role in allergic airway inflammation, suggesting different functions between BLT1 and BLT2 in the pathogenesis of asthma. Selective BLT1 antagonists may have a potential therapeutic application in patients with asthma, and BLT2 may represent a novel therapeutic target for lung diseases.</p> </abstract>