Background
Eicosanoids are arachidonic acid-derived mediators that play a key role in the regulation of inflammatory response. 5-Lipoxygenase (5-LOX)-derived leukotrienes are considered proinflammatory while 15-lipoxygenase (15-LOX)-derived products such as 15-hydroxyeicosatetraenoic acid (15-HETE) and lipoxins inhibit proinflammatory mediators including leukotrienes, and actively participate in the resolution of inflammation. It has been demonstrated that a temporal switch of arachidonic acid metabolism from predominant 5-LOX-derived to 15-LOX-derived products is crucial for the resolution of inflammation. We have recently shown that there is an imbalance between proinflammatory leukotrienes and anti-inflammatory lipoxins in the lungs of patients with systemic sclerosis (SSc)-related interstitial lung disease, which may favour chronic inflammation and fibrosis [1, 2].