Details:

Alternative Title:
PLoS One
Personal Author:
Badding, Melissa A. ; Schwegler-Berry, Diane ; Park, Ju-Hyeong ; Fix, Natalie R. ; Cummings, Kristin J. ; ... More +
Badding, Melissa A. ; Schwegler-Berry, Diane ; Park, Ju-Hyeong ; Fix, Natalie R. ; Cummings, Kristin J. ; Leonard, Stephen S. Less -
Description:
Indium-tin oxide (ITO) is used to make transparent conductive coatings for touch-screen and liquid crystal display electronics. As the demand for consumer electronics continues to increase, so does the concern for occupational exposures to particles containing these potentially toxic metal oxides. Indium-containing particles have been shown to be cytotoxic in cultured cells and pro-inflammatory in pulmonary animal models. In humans, pulmonary alveolar proteinosis and fibrotic interstitial lung disease have been observed in ITO facility workers. However, which ITO production materials may be the most toxic to workers and how they initiate pulmonary inflammation remain poorly understood. Here we examined four different particle samples collected from an ITO production facility for their ability to induce pro-inflammatory responses in vitro. Tin oxide, sintered ITO (SITO), and ventilation dust particles activated nuclear factor kappa B (NFκB) within 3 h of treatment. However, only SITO induced robust cytokine production (IL-1β, IL-6, TNFα, and IL-8) within 24 h in both RAW 264.7 mouse macrophages and BEAS-2B human bronchial epithelial cells. Our lab and others have previously demonstrated SITO-induced cytotoxicity as well. These findings suggest that SITO particles activate the NLRP3 inflammasome, which has been implicated in several immune-mediated diseases via its ability to induce IL-1β release and cause subsequent cell death. Inflammasome activation by SITO was confirmed, but it required the presence of endotoxin. Further, a phagocytosis assay revealed that pre-uptake of SITO or ventilation dust impaired proper macrophage phagocytosis of E. coli. Our results suggest that adverse inflammatory responses to SITO particles by both macrophage and epithelial cells may initiate and propagate indium lung disease. These findings will provide a better understanding of the molecular mechanisms behind an emerging occupational health issue.
Subjects:
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Animals Carrier Proteins Cell Line Chemical Industry Endotoxins Epithelial Cells Escherichia Coli Gene Expression Regulation Humans Inflammasomes Interleukin-1beta Interleukin-6 Interleukin-8 Macrophages Mice NF-kappa B NLR Family, Pyrin Domain-Containing 3 Protein Occupational Exposure Particle Size Phagocytosis Signal Transduction Tin Compounds Tumor Necrosis Factor-alpha
Source:
PLoS One. 10(4).
Document Type:
Journal Article
Collection(s):
CDC Public Access
Main Document Checksum:
[+]
urn:sha256:476fb69d1567eca6e0d3d337681699df62cd415562eefc91d5c441179d1cf408
Download URL:
https://stacks.cdc.gov/view/cdc/30621/cdc_30621_DS1.pdf
File Type:

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