A turn on and a turn off: BLT1 and BLT2 mechanisms in the lung

Expert Rev Respir Med. 2014 Aug;8(4):381-3. doi: 10.1586/17476348.2014.908715. Epub 2014 Apr 18.

Abstract

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.

Keywords: BLT1; BLT2; LTB4; lung disease.

Publication types

  • Editorial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Asthma / metabolism*
  • Asthma / pathology
  • Humans
  • Leukotriene B4 / metabolism*
  • Lung / metabolism*
  • Lung / pathology
  • Receptors, Leukotriene B4 / metabolism*
  • Signal Transduction / physiology

Substances

  • LTB4R protein, human
  • LTB4R2 protein, human
  • Receptors, Leukotriene B4
  • Leukotriene B4