1. Small airway epithelial cells exposure to printer-emitted engineered nanoparticles induces cellular effects on human microvascular endothelial cells in an alveolar-capillary co-culture model.
- Author
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Sisler JD, Pirela SV, Friend S, Farcas M, Schwegler-Berry D, Shvedova A, Castranova V, Demokritou P, and Qian Y
- Subjects
- Air Pollutants chemistry, Capillaries cytology, Capillaries drug effects, Capillaries immunology, Cell Line, Cell Survival drug effects, Coculture Techniques, Cytokines metabolism, Dose-Response Relationship, Drug, Endothelial Cells immunology, Endothelial Cells pathology, Endothelium, Vascular drug effects, Endothelium, Vascular immunology, Endothelium, Vascular pathology, Epithelial Cells drug effects, Epithelial Cells immunology, Epithelial Cells pathology, Humans, Microscopy, Confocal, Microvessels immunology, Microvessels pathology, Nanoparticles chemistry, Particle Size, Pulmonary Alveoli drug effects, Pulmonary Alveoli immunology, Pulmonary Alveoli pathology, Respiratory Mucosa blood supply, Respiratory Mucosa immunology, Respiratory Mucosa pathology, Surface Properties, Air Pollutants toxicity, Endothelial Cells drug effects, Microvessels drug effects, Nanoparticles toxicity, Printing, Respiratory Mucosa drug effects
- Abstract
The printer is one of the most common office equipment. Recently, it was reported that toner formulations for printing equipment constitute nano-enabled products (NEPs) and contain engineered nanomaterials (ENMs) that become airborne during printing. To date, insufficient research has been performed to understand the potential toxicological properties of printer-emitted particles (PEPs) with several studies using bulk toner particles as test particles. These studies demonstrated the ability of toner particles to cause chronic inflammation and fibrosis in animal models. However, the toxicological implications of inhalation exposures to ENMs emitted from laser printing equipment remain largely unknown. The present study investigates the toxicological effects of PEPs using an in vitro alveolar-capillary co-culture model with Human Small Airway Epithelial Cells (SAEC) and Human Microvascular Endothelial Cells (HMVEC). Our data demonstrate that direct exposure of SAEC to low concentrations of PEPs (0.5 and 1.0 µg/mL) caused morphological changes of actin remodeling and gap formations within the endothelial monolayer. Furthermore, increased production of reactive oxygen species (ROS) and angiogenesis were observed in the HMVEC. Analysis of cytokine and chemokine levels demonstrates that interleukin (IL)-6 and MCP-1 may play a major role in the cellular communication observed between SAEC and HMVEC and the resultant responses in HMVEC. These data indicate that PEPs at low, non-cytotoxic exposure levels are bioactive and affect cellular responses in an alveolar-capillary co-culture model, which raises concerns for potential adverse health effects.
- Published
- 2015
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