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ToxSci Advance Access published online on June 19, 2007
Toxicological Sciences, doi:10.1093/toxsci/kfm145
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© The Author 2007. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Immunomodulatory Effects of Oak Dust Exposure in a Murine Model of Allergic Asthma

Juha Määttä1,*, Rita Haapakoski1,*, Maili Lehto1, Marina Leino1, Sari Tillander1, Kirsti Husgafvel-Pursiainen2, Henrik Wolff2,3, Kai Savolainen4 and Harri Alenius1

1 Unit of Excellence in Immunotoxicology, Finnish Institute of Occupational Health, Helsinki, Finland 2 Team for Biological Mechanisms and Prevention of Work-related Diseases, Finnish Institute of Occupational Health, Helsinki, Finland 3 Department of Pathology, Helsinki University Central Hospital, Finland 4 New Technologies and Risk Analysis, Finnish Institute of Occupational Health, Helsinki, Finland

Address correspondence to: Harri Alenius, PhD, Finnish Institute of Occupational Health, Topeliuksenkatu 41 a A, FIN-00250 Helsinki, Finland. Tel. (358)-30-4742175, Fax (358)-30-4742116, Email: Harri.Alenius{at}ttl.fi

Received May 2, 2007; revision received May 29, 2007; accepted May 30, 2007


  Abstract

Repeated airway exposure to wood dust has been reported to cause adverse respiratory effects such as asthma and chronic bronchitis. In our recent study we found that exposure of mice to oak dust induced more vigorous lung inflammation compared to birch dust exposure. In the present study we assessed the immunomodulatory effects of repeated intranasal exposure to oak dust both in non-allergic and in ovalbumin-sensitized, allergic mice. Allergen induced influx of eosinophils and lymphocytes was seen in the lungs of allergic mice. Oak dust exposure elicited infiltration of neutrophils, lymphocytes and macrophages in non-allergic mice. Interestingly, oak dust-induced lung neutrophilia as well as oak dust induced production of the proinflammatory cytokine TNF-{alpha} and chemokine CCL3 was significantly suppressed in allergic mice. On the other hand, allergen induced expression of IL-13 mRNA and protein was significantly reduced in oak dust exposed allergic mice. Finally, allergen induced airway hyperreactivity to inhaled metacholine was significantly suppressed in oak dust exposed allergic mice. The present results suggest that repeated airway exposure to oak dust can regulate pulmonary inflammation and airways responses depending on the immunological status of the animal.

Key Words: Wood dust; Inflammation; Asthma; Lung; Cytokine.

* Equal contribution


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