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ToxSci Advance Access originally published online on June 19, 2007
Toxicological Sciences 2007 99(1):260-266; 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 Määttä*,1, Rita Haapakoski*,1, Maili Lehto*, Marina Leino*, Sari Tillander*, Kirsti Husgafvel-Pursiainen{dagger}, Henrik Wolff{dagger},{ddagger}, Kai Savolainen§ and Harri Alenius*,2

* Unit of Excellence in Immunotoxicology {dagger} Team for Biological Mechanisms and Prevention of Work-related Diseases {ddagger} New Technologies and Risk Analysis, Finnish Institute of Occupational Health, Topeliuksenkatu 41 a A, FIN-00250, Helsinki, Finland § Department of Pathology, Helsinki University Central Hospital, Helsinki, Finland

2 To whom correspondence should be addressed. Fax: +358-30-4742116. E-mail: harri.alenius{at}ttl.fi.

Received May 2, 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 nonallergic 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 nonallergic mice. Interestingly, oak dust–induced lung neutrophilia as well as oak dust–induced production of the proinflammatory cytokine TNF-{alpha} and chemokine CCL3 were 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 airway responses depending on the immunological status of the animal.

Key Words: wood dust; inflammation; asthma; lung; cytokine.

1 These authors contributed equally to this study.


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