title: Mechanisms of particle-induced pulmonary inflammation in a mouse model: exposure to wood dust.
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 < 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.
authors.affiliation: Department of Industrial Hygiene and Toxicology, Department of Occupational Medicine, and Lappeenranta Regional Institute of Occupational Health, Lappeenranta, Finland.
authors.forename: Juha
authors.initials: J
authors.lastname: Määttä
authors.forename: Maili
authors.initials: M
authors.lastname: Lehto
authors.forename: Marina
authors.initials: M
authors.lastname: Leino
authors.forename: Sari
authors.initials: S
authors.lastname: Tillander
authors.forename: Rita
authors.initials: R
authors.lastname: Haapakoski
authors.forename: Marja-Leena
authors.initials: ML
authors.lastname: Majuri
authors.forename: Henrik
authors.initials: H
authors.lastname: Wolff
authors.forename: Sari
authors.initials: S
authors.lastname: Rautio
authors.forename: Irma
authors.initials: I
authors.lastname: Welling
authors.forename: Kirsti
authors.initials: K
authors.lastname: Husgafvel-Pursiainen
authors.forename: Kai
authors.initials: K
authors.lastname: Savolainen
authors.forename: Harri
authors.initials: H
authors.lastname: Alenius
mesh_terms: 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
chemical_list: D016207:Cytokines; D017931:DNA Primers; D004391:Dust; D019707:Receptors, Chemokine; D016210:Methacholine Chloride