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12/15-Lipoxygenase deficiency protects mice from allergic airways inflammation and increases secretory IgA levels.

Authors: Hajek, AR  Lindley, AR  Favoreto S, JR  Carter, R  Schleimer, RP  Kuperman, DA 
Citation: Hajek AR, etal., J Allergy Clin Immunol. 2008 Sep;122(3):633-9.e3. Epub 2008 Aug 9.
Pubmed: (View Article at PubMed) PMID:18692885
DOI: Full-text: DOI:10.1016/j.jaci.2008.06.021

BACKGROUND: Induction of 15-lipoxygenase-1 (15-LO-1) has been observed in the airways of subjects with asthma, although its physiologic role in the airways has remained largely undefined. OBJECTIVES: We sought to test the hypothesis that the mouse 15-LO-1 ortholog 12/15-LO contributes to the development of allergic airways inflammation. METHODS: Two models were used to evaluate wild-type and 12/15-LO-deficient mice. The systemic model involved intraperitoneal injections of allergen, and the mucosal model involved allergen exposures occurring exclusively in the airways. The systemic and mucosal-specific contributions of 12/15-LO to allergic sensitization and airways inflammation were determined by comparing the results obtained in the 2 models. RESULTS: In the mucosal model 12/15-LO knockout mice were protected from the development of allergic sensitization and airways inflammation, as evidenced by circulating levels of allergen-specific IgE, IgG1, and IgG2a; the profile of inflammatory cells in bronchoalveolar lavage fluid; and the expression of cytokines and mediators in lung tissue. In the systemic model 12/15-LO knockout mice were not protected. This suggested the presence of a lung-restricted protective role for 12/15-LO deficiency that was potentially accounted for by increased activation of mucosal B cells and increased production of the known mucosal-specific protective mediator secretory IgA. CONCLUSIONS: Induction of 15-LO-1 in asthma might contribute to allergic sensitization and airways inflammation, potentially by causing suppression of secretory IgA.

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CRRD Object Information
CRRD ID: 5509784
Created: 2011-11-03
Species: All species
Last Modified: 2011-11-03
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.