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Mediators of Inflammation
Volume 2010 (2010), Article ID 727305, 10 pages
Research Article

12/15-Lipoxygenase Is an Interleukin-13 and Interferon- Counterregulated-Mediator of Allergic Airway Inflammation

Allergy-Immunology Division, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA

Received 6 May 2010; Revised 10 July 2010; Accepted 16 September 2010

Academic Editor: Alex Kleinjan

Copyright © 2010 Alexa R. Lindley et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Interleukin-13 and interferon- are important effectors of T-helper cells. Interleukin-13 increases expression of the arachidonic acid-metabolizing enzyme, 15-lipoxygenase-1, in a variety of cell types. 15-lipoxygenase-1 is dramatically elevated in the airways of subjects with asthma. Studies in animals indicate that 15-lipoxygenase-1 contributes to the development of allergic airway inflammation but is protective in some other forms of inflammation. We tested the hypothesis that the ability of interleukin-13 and interferon- to counterregulate allergic airway inflammation was potentially mediated by counterregulation of 12/15-lipoxygenase, the mouse ortholog of 15-lipoxygenase-1. The airways of mice were treated with interleukin-13 or interferon- one day prior to each of the four allergen exposures. Interleukin-13 augmented and interferon- inhibited allergic airway inflammation independently of systemic IgE and mucosal IgA responses but in association with counterregulation of 12/15-lipoxygenase. Interleukin-13 and interferon- counterregulate 12/15-lipoxygenase potentially contributing to the effects of these cytokines on allergic airway inflammation.