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ToxSci Advance Access published online on June 1, 2006
Toxicological Sciences, doi:10.1093/toxsci/kfl026
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© The Author 2006. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received December 22, 2005
Accepted May 23, 2006

Genetic Toxicology

Mechanisms of Particle-Induced Pulmonary Inflammation in a Mouse Model: Exposure to Wood Dust

Juha Määttä MSc 1, Maili Lehto MSc 1, Marina Leino MSc 1, Sari Tillander BSc 1, Rita Haapakoski MSc 1, Marja-Leena Majuri PhD 1, Henrik Wolff MD 2, Sari Rautio MSc(Eng) 3, Irma Welling PhD 3, Kirsti Husgafvel-Pursiainen PhD 1, Kai Savolainen MD 1, and Harri Alenius PhD 1 *

1 From Department of Industrial Hygiene and Toxicology, Finnish Institute of Occupational Health, Helsinki, Finland
2 From Department of Occupational Medicine, Finnish Institute of Occupational Health, Helsinki, Finland
3 From Department of Lappeenranta Regional Institute of Occupational Health, Lappeenranta, Finnish Institute of Occupational Health, Helsinki, Finland

* To whom correspondence should be addressed.
Harri Alenius, E-mail: Harri.Alenius{at}ttl.fi


  Abstract

Repeated airway exposure to wood dust has long been known to cause adverse respiratory effects such as asthma and chronic bronchitis and impairment of lung function. However, the mechanisms underlying the inflammatory responses of the airways after wood dust exposure are poorly known. We used a mouse model to elucidate the mechanisms of particle-induced inflammatory responses to fine wood dust particles. BALB/c mice were exposed to intranasally administered fine (more than 99% of the particles had a particle size of ≤ 5 µm, with virtually identical size distribution) birch or oak dusts twice a week for three weeks. PBS, LPS and titanium dioxide were used as controls. Intranasal installation of birch or oak dusts elicited influx of inflammatory cells to the lungs in mice. Enhancement of lymphocytes and neutrophils was seen after oak dust exposure, whereas eosinophil infiltration was higher after birch dust exposure. Infiltration of inflammatory cells was associated with an increase in the mRNA levels of several cytokines, chemokines, and chemokine receptors in lung tissue. Oak dust appeared to be a more potent inducer of these inflammatory mediators than birch dust. The results from our in vivo mouse model show that repeated airway exposure to wood dust can elicit lung inflammation which is accompanied by induction of several pro-inflammatory cytokines and chemokines. Oak and birch dusts exhibited quantitative and qualitative differences in the elicitation of pulmonary inflammation, suggesting that the inflammatory responses induced by the wood species may rise via different cellular mechanisms.

Keywords: Chemokines; cytokines; gene expression; leukocytes.
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J. Maatta, R. Haapakoski, M. Lehto, M. Leino, S. Tillander, K. Husgafvel-Pursiainen, H. Wolff, K. Savolainen, and H. Alenius
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