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The Journal of Immunology, 2000, 164: 2267-2271.
Copyright © 2000 by The American Association of Immunologists

CUTTING EDGE

Cutting Edge: Lipoxin (LX) A4 and Aspirin-Triggered 15-Epi-LXA4 Block Allergen-Induced Eosinophil Trafficking1

Christianne Bandeira-Melo*, Patricia T. Bozza2,*, Bruno L. Diaz*, Renato S. B. Cordeiro*, Peter J. Jose{dagger}, Marco A. Martins* and Charles N. Serhan{ddagger}

* Department of Physiology and Pharmacodynamics, Oswaldo Cruz Institute, Fundaçao Oswaldo Cruz, Rio de Janeiro, Brazil; {dagger} Leucocyte Biology, Biomedical Sciences Division, Imperial College School of Medicine, London, United Kingdom; and {ddagger} Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women’s Hospital, Boston, MA 02115

Tissue eosinophilia prevention represents one of the primary targets to new anti-allergic therapies. As lipoxin A4 (LXA4) and aspirin-triggered 15-epi-LXA4 (ATL) are emerging as endogenous "stop signals" produced in distinct pathologies including some eosinophil-related pulmonary disorders, we evaluated the impact of in situ LXA4/ATL metabolically stable analogues on allergen-induced eosinophilic pleurisy in sensitized rats. LXA4/ATL analogues dramatically blocked allergic pleural eosinophil influx, while concurrently increasing circulating eosinophilia, inhibiting the earlier edema and neutrophilia associated with allergic reaction. The mechanisms underlying this LXA4/ATL-driven allergic eosinophilia blockade was independent of mast cell degranulation and involved LXA4/ATL inhibition of both IL-5 and eotaxin generation, as well as platelet activating factor action. These findings reveal LXA4/ATL as a novel class of endogenous anti-allergic mediators, capable of preventing local eosinophilia.




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