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The Inflammatory Effect of Iron Oxide and Silica Particles on Lung Epithelial Cells
1School of Medicine, University of Tasmania, 17 Liverpool St, Hobart, TAS, 7000, Australia.
Purpose:
Our understanding of the respiratory health consequences of geogenic (earth-derived) particulate matter (PM) is limited. Recent in vivo evidence suggests that the concentration of iron is associated with the magnitude of the respiratory response to geogenic PM. We investigated the inflammatory and cytotoxic potential of silica and iron oxide particles alone, and in combination, on lung epithelial cells.
Methods:
Bronchial epithelial cells (BEAS-2B) were exposed to silica (quartz, cristobalite) and/or iron oxide (hematite, magnetite) particles. Cytotoxicity and cytokine production (IL-6, IL-8, IL-1β and TNF-α) were assessed by LDH assay and ELISA, respectively. In subsequent experiments, the cytotoxic and inflammatory potential of the particles was assessed using alveolar epithelial cells (A549).
Results:
After 24 h of exposure, iron oxide did not cause significant cytotoxicity or production of cytokines, nor did it augment the response of silica in the BEAS2-B cells. In contrast, while the silica response was not augmented in the A549 cells by the addition of iron oxide, iron oxide particles alone were sufficient to induce IL-8 production in these cells. There was no response detected for any of the outcomes at the 4 h time point, nor was there any evidence of IL-1β or TNF-α production.
Conclusions:
While previous studies have suggested that iron may augment silica-induced inflammation, we saw no evidence of this in human epithelial cells. We found that alveolar epithelial cells produce pro-inflammatory cytokines in response to iron oxide particles, suggesting that previous in vivo observations are due to the alveolar response to these particles.
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