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Inflammatory response in human alveolar epithelial cells after TiO NPs or ZnO NPs exposure: Inhibition of surfactant protein A expression as an indicator for loss of lung function.
Jiménez-Chávez, A Solorio-Rodríguez, A Escamilla-Rivera, V Leseman, D Morales-Rubio, R Uribe-Ramírez, M Campos-Villegas, L Medina-Ramírez, I E Arreola-Mendoza, L Cassee, F R
Jiménez-Chávez, A
Solorio-Rodríguez, A
Escamilla-Rivera, V
Leseman, D
Morales-Rubio, R
Uribe-Ramírez, M
Campos-Villegas, L
Medina-Ramírez, I E
Arreola-Mendoza, L
Cassee, F R
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Open Access
Type
Article
Language
en
Date
2021-04-03
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Title
Inflammatory response in human alveolar epithelial cells after TiO NPs or ZnO NPs exposure: Inhibition of surfactant protein A expression as an indicator for loss of lung function.
Translated Title
Published in
Environ Toxicol Pharmacol 2021; 103654 advance online publication (ahead of print)
Abstract
The increasing use of metal oxide nanoparticles (MONPs) as TiO2 NPs or ZnO NPs has led to environmental release and human exposure. The respiratory system, effects on lamellar bodies and surfactant protein A (SP-A) of pneumocytes, can be importantly affected. Exposure of human alveolar epithelial cells (A549) induced differential responses; a higher persistence of TiO2 in cell surface and uptake (measured by Atomic Force Microscopy) and sustained inflammatory response (by means of TNF-α, IL-10, and IL-6 release) and ROS generation were observed, whereas ZnO showed a modest response and low numbers in cell surface. A reduction in SP-A levels at 24 h of exposure to TiO2 NPs (concentration-dependent) or ZnO NPs (the higher concentration) was also observed, reversed by blocking the inflammatory response (by the inhibition of IL-6). Loss of SP-A represents a relevant target of MONPs-induced inflammatory response that could contribute to cellular damage and loss of lung function.