Asthma is a chronic airway inflammatory disease characterized by an infiltration of inflammatory cells, including eosinophils, mast cells, and T lymphocytes.1 x 1. Bousquet, J., Chanez, P., Lacoste, J.Y., Barneon, G., Ghavanian, N., Enander, I. et al. Eosinophilic inflammation in asthma. N Engl J Med. 1990; 323: 1033–1039 Crossref | PubMed | Scopus (1964) | Google Scholar See all References Leukotrienes (LTs), lipid mediators generated from arachidonic acid by the action of 5-lipoxygenase, play important roles in the pathogenesis of allergic airway inflammation.2 x 2. Barnes, P.J., Chung, K.F., and Page, C.P. Inflammatory mediators of asthma: an update. Pharmacol Rev. 1998; 50: 515–596 PubMed | Google Scholar See all References LTC4, LTD4, and LTE4, known as cysteinyl leukotrienes (cysLTs), are both direct bronchoconstrictors and proinflammatory substances and are involved in recruitment of inflammatory cells, airway smooth muscle contraction, vascular leakage, increased mucus secretion, and decreased mucociliary clearance.3 x 3. Busse, W.W. Leukotrienes and inflammation. Am J Respir Crit Care Med. 1998; 157: 210S–213S Crossref | PubMed | Google Scholar See all References cysLTs are shown to cause plasma extravasation in in vivo and in vitro studies.4. x 4. Drazen, J.M., Austen, K.F., Lewis, R.A., Clark, D.A., Goto, G., Marfat, A. et al. Comparative airway and vascular activities of leukotrienes C-1 and D in vivo and in vitro. Proc Natl Acad Sci U S A. 1980; 77: 4354–4358 Crossref | PubMed | Scopus (501) | Google Scholar See all References ,5. x 5. Hedqvist, P., Dahlen, S.E., Gustafsson, L., Hammarstrom, S., and Samuelsson, B. Biological profile of leukotrienes C4 and D4. Acta Physiol Scand. 1980; 110: 331–333 Crossref | PubMed | Scopus (179) | Google Scholar See all References ,6. x 6. Camp, R.D., Coutts, A.A., Greaves, M.W., Kay, A.B., and Walport, M.J. Responses of human skin to intradermal injection of leukotrienes C4, D4 and B4. Br J Pharmacol. 1983; 80: 497–502 Crossref | PubMed | Scopus (179) | Google Scholar See all References ,7. x 7. Soter, N.A., Lewis, R.A., Corey, E.J., and Austen, K.F. Local effects of synthetic leukotrienes (LTC4, LTD4, LTE4, and LTB4) in human skin. J Invest Dermatol. 1983; 80: 115–119 Crossref | PubMed | Scopus (412) | Google Scholar See all References ,8. x 8. Evans, T.W., Rogers, D.F., Aursudkij, B., Chung, K.F., and Barnes, P.J. Regional and time-dependent effects of inflammatory mediators on airway microvascular permeability in the guinea pig. Clin Sci. 1989; 76: 479–485 PubMed | Google Scholar See all References ,9. x 9. Henderson, W.R. Jr. The role of leukotrienes in asthma. Ann Allergy. 1994; 72: 272–278 PubMed | Google Scholar See all References ,10. x 10. Arakawa, H., Lotvall, J., Kawikova, I., Lofdahl, C.G., and Skoogh, B.E. Leukotriene D4- and prostaglandin F2 alpha-induced airflow obstruction and airway plasma exudation in guinea-pig: role of thromboxane and its receptor. Br J Pharmacol. 1993; 110: 127–132 Crossref | PubMed | Scopus (28) | Google Scholar See all References Inflammation of the asthmatic airway is usually accompanied by increased vascular permeability and plasma exudation. However, the mechanisms by which cysLTs induce increased vascular permeability are not clearly understood.