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

Proinflammatory cytokine Infiltration (HVAC) Inhalation exposure Cellular infiltration
DOI: 10.1093/toxsci/kfl026 Publication Date: 2006-06-02T00:39:34Z
ABSTRACT
Repeated airway exposure to wood dust has long been known cause adverse respiratory effects such as asthma and chronic bronchitis impairment of lung function. However, the mechanisms underlying inflammatory responses airways after are poorly known. We used a mouse model elucidate particle-induced fine particles. BALB/c mice were exposed intranasally administered (more than 99% particles had particle size ≤ 5 μm, with virtually identical distribution) birch or oak dusts twice week for 3 weeks. PBS, LPS, titanium dioxide controls. Intranasal instillation elicited influx cells lungs in mice. Enhancement lymphocytes neutrophils was seen exposure, whereas eosinophil infiltration higher exposure. Infiltration associated an increase mRNA levels several cytokines, chemokines, chemokine receptors tissue. Oak appeared be more potent inducer these mediators dust. The results from our vivo show that repeated can elicit inflammation, which is accompanied by induction proinflammatory cytokines chemokines. exhibited quantitative qualitative differences elicitation pulmonary suggesting induced species may rise via different cellular mechanisms.
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