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γ‐Tocopherol prevents airway eosinophilia and mucous cell hyperplasia in experimentally induced allergic rhinitis and asthma
Author(s) -
Wagner J. G.,
Jiang Q.,
Harkema J. R.,
Ames B. N.,
Illek B.,
Roubey R. A.,
Peden D. B.
Publication year - 2008
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.2007.02855.x
Subject(s) - medicine , immunology , provocation test , eosinophil , allergic inflammation , eosinophilia , prostaglandin d2 , house dust mite , goblet cell , bronchoalveolar lavage , allergy , asthma , allergen , pathology , lung , prostaglandin , epithelium , alternative medicine
Summary Background Traditional therapies for asthma and allergic rhinitis (AR) such as corticosteroids and antihistamines are not without limitations and side effects. The use of complementary and alternative approaches to treat allergic airways disease, including the use of herbal and dietary supplements, is increasing but their efficacy and safety are relatively understudied. Previously, we have demonstrated that γ‐tocopherol (γT), the primary form of dietary vitamin E, is more effective than α‐tocopherol, the primary form found in supplements and tissue, in reducing systemic inflammation induced by non‐immunogenic stimuli. Objective We used allergic Brown Norway rats to test the hypothesis that a dietary supplement with γT would protect from adverse nasal and pulmonary responses to airway allergen provocation. Methods Ovalbumin (OVA)‐sensitized Brown Norway rats were treated orally with γT before intranasal provocation with OVA. Twenty‐four hours after two challenges, histopathological changes in the nose, sinus and pulmonary airways were compared with gene expression and cytokine production in bronchoalveolar lavage fluid and plasma. Results We found that acute dosing for 4 days with γT was sufficient to provide broad protection from inflammatory cell recruitment and epithelial cell alterations induced by allergen challenge. Eosinophil infiltration into airspaces and tissues of the lung, nose, sinus and nasolacrimal duct was blocked in allergic rats treated with γT. Pulmonary production of soluble mediators PGE 2 , LTB 4 and cysteinyl leukotrienes, and nasal expression of IL‐4, ‐5, ‐13 and IFN‐γ were also inhibited by γT. Mucous cell metaplasia, the increase in the number of goblet cells and amounts of intraepithelial mucus storage, was induced by allergen in both pulmonary and nasal airways and decreased by treatment with γT. Conclusions Acute treatment with γT inhibits important inflammatory pathways that underlie the pathogenesis of both AR and asthma. Supplementation with γT may be a novel complementary therapy for allergic airways disease.