Mechanisms of particle-induced pulmonary inflammation in a mouse model: exposure to wood dust.
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 < or = 5 microm, with virtually identical size distribution) birch or oak dusts twice a week for 3 weeks. PBS, LPS, and titanium dioxide were used as controls. Intranasal instillation 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 proinflammatory 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.
Määttä
Juha
J
Department of Industrial Hygiene and Toxicology, Department of Occupational Medicine, and Lappeenranta Regional Institute of Occupational Health, Lappeenranta, Finland.
Lehto
Maili
M
Leino
Marina
M
Tillander
Sari
S
Haapakoski
Rita
R
Majuri
Marja-Leena
ML
Wolff
Henrik
H
Rautio
Sari
S
Welling
Irma
I
Husgafvel-Pursiainen
Kirsti
K
Savolainen
Kai
K
Alenius
Harri
H
D000818:Animals; D001483:Base Sequence; D001980:Bronchi / Q000187:drug effects / Q000503:physiopathology; D016207:Cytokines / Q000378:metabolism; D017931:DNA Primers; D004391:Dust; D005260:Female; D008168:Lung / Q000378:metabolism; D016210:Methacholine Chloride / Q000008:administration & dosage; D051379:Mice; D008807:Mice, Inbred BALB C; D011014:Pneumonia / Q000209:etiology* / Q000378:metabolism; D019707:Receptors, Chemokine / Q000378:metabolism; D014934:Wood
D016207:Cytokines; D017931:DNA Primers; D004391:Dust; D019707:Receptors, Chemokine; D016210:Methacholine Chloride