Abstract
Nanoparticle exposure by accidental inhalation is increasing due to broad use in consumer and industrial products. We demonstrated a rapid eosinophilia following acute pulmonary exposure to long single wall carbon nanotubes (SWCNT). With the hypothesis that SWCNT are creating damage‐associated molecular patterns (DAMPs) in response to pulmonary exposure, 15 rats were intratracheally given either 50 μL surfactant containing 500 μg/mL SWCNT or surfactant. Sterility was determined by limulus lysate assay. Bronchoalveolar lavage (BAL), serum and tissue were harvested acutely (0.5 – 24 hr) or subchronically (1–4 wk). DAMP‐related proteins (high mobility box protein‐1 HMGB1 and heat shock protein‐70 HSP70), a receptor (RAGE), and TNFα were measured. BAL DAMP molecules and TNFα were elevated acutely vs subchronically (p=0.02) with HMGB1 and TNFα peaking at 30 min (34.7 and 36.7 pg/mL respectively, 4 times the surfactant controls). A robust lung tissue eosinophilia, 20 cells per field at 400x, was also seen at 30 min. RAGE receptors were widely upregulated in tissue as determined by immunostaining, strong at 24 hours. At 1–4 weeks granulomas were seen around particle clusters visible by light microscopy, and DAMP molecules and TNFα decreased in BAL to ~1/3 the acute titers. All markers increased again at 4 weeks, suggesting macrophage necrosis and secondary SWCNT release.Funding: St. Luke's Foundation, Kansas City
Published Version
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