Lipoxins in asthma: potential therapeutic mediators on bronchial inflammation?
Article first published online: 7 SEP 2004
Volume 59, Issue 10, pages 1027–1041, October 2004
How to Cite
Bonnans, C., Chanez, P. and Chavis, C. (2004), Lipoxins in asthma: potential therapeutic mediators on bronchial inflammation?. Allergy, 59: 1027–1041. doi: 10.1111/j.1398-9995.2004.00617.x
- Issue published online: 7 SEP 2004
- Article first published online: 7 SEP 2004
- Accepted for publication 15 April 2004
- transcellular metabolism
Arachidonic acid metabolism represents an important source of mediators with ambivalent actions. Among these, lipoxins (LXs) are the first agents identified and recognized as anti-inflammatory endogenous lipid mediators, which are involved in the resolution of inflammation and are present in the airways of asthmatic patients. Lipoxins result mainly from the interaction between 5 and 15-lipoxygenases (LO) and their levels are modulated by the degree of bronchial inflammation as well as by the long-term glucocorticoid treatments. In the airways, LX synthesis is higher in mild asthmatics than in severe asthmatics, whereas in vitro chemokine release inhibition by LXs is more effective in cells from severe asthmatics than from mild asthmatics. LipoxinA4 effects on interleukin (IL)-8 released by blood mononuclear cells and on calcium influx in epithelial cells are mediated by the specific receptor ALX. Lipoxin generation by lung epithelial cells depends mainly on 15-LO activity. Mild asthmatics present higher 15-LOb expression at the epithelium level than severe patients, whereas the LX deficit in severe asthma is associated with an up-regulation of the 15-LOa expressions. Therefore, bronchial epithelial cells become a target for therapeutic intervention and LXs represent a potential therapeutic solution for bronchial inflammation resolution in asthma.