Pulmonary surfactant augments cytotoxicity of silica nanoparticles: Studies on an in vitro air–blood barrier model
The air–blood barrier is a very thin membrane of about 2.2 µm thickness and therefore represents an ideal portal of entry for nanoparticles to be used therapeutically in a regenerative medicine strategy. Until now, numerous studies using cellular airway models have been conducted in vitro in order t...
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Beilstein-Institut
2015-02-01
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Series: | Beilstein Journal of Nanotechnology |
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Online Access: | https://doi.org/10.3762/bjnano.6.54 |
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author | Jennifer Y. Kasper Lisa Feiden Maria I. Hermanns Christoph Bantz Michael Maskos Ronald E. Unger C. James Kirkpatrick |
author_facet | Jennifer Y. Kasper Lisa Feiden Maria I. Hermanns Christoph Bantz Michael Maskos Ronald E. Unger C. James Kirkpatrick |
author_sort | Jennifer Y. Kasper |
collection | DOAJ |
description | The air–blood barrier is a very thin membrane of about 2.2 µm thickness and therefore represents an ideal portal of entry for nanoparticles to be used therapeutically in a regenerative medicine strategy. Until now, numerous studies using cellular airway models have been conducted in vitro in order to investigate the potential hazard of NPs. However, in most in vitro studies a crucial alveolar component has been neglected. Before aspirated NPs encounter the cellular air–blood barrier, they impinge on the alveolar surfactant layer (10–20 nm in thickness) that lines the entire alveolar surface. Thus, a prior interaction of NPs with pulmonary surfactant components will occur. In the present study we explored the impact of pulmonary surfactant on the cytotoxic potential of amorphous silica nanoparticles (aSNPs) using in vitro mono- and complex coculture models of the air–blood barrier. Furthermore, different surface functionalisations (plain-unmodified, amino, carboxylate) of the aSNPs were compared in order to study the impact of chemical surface properties on aSNP cytotoxicity in combination with lung surfactant. The alveolar epithelial cell line A549 was used in mono- and in coculture with the microvascular cell line ISO-HAS-1 in the form of different cytotoxicity assays (viability, membrane integrity, inflammatory responses such as IL-8 release). At a distinct concentration (100 µg/mL) aSNP–plain displayed the highest cytotoxicity and IL-8 release in monocultures of A549. aSNP–NH2 caused a slight toxic effect, whereas aSNP–COOH did not exhibit any cytotoxicity. In combination with lung surfactant, aSNP–plain revealed an increased cytotoxicity in monocultures of A549, aSNP–NH2 caused a slightly augmented toxic effect, whereas aSNP–COOH did not show any toxic alterations. A549 in coculture did not show any decreased toxicity (membrane integrity) for aSNP–plain in combination with lung surfactant. However, a significant augmented IL-8 release was observed, but no alterations in combination with lung surfactant. The augmented aSNP toxicity with surfactant in monocultures appears to depend on the chemical surface properties of the aSNPs. Reactive silanol groups seem to play a crucial role for an augmented toxicity of aSNPs. The A549 cells in the coculture seem to be more robust towards aSNPs, which might be a result of a higher differentiation and polarization state due the longer culture period. |
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spelling | doaj.art-5cc9b91589444cf688ef64a0613440992022-12-21T18:14:28ZengBeilstein-InstitutBeilstein Journal of Nanotechnology2190-42862015-02-016151752810.3762/bjnano.6.542190-4286-6-54Pulmonary surfactant augments cytotoxicity of silica nanoparticles: Studies on an in vitro air–blood barrier modelJennifer Y. Kasper0Lisa Feiden1Maria I. Hermanns2Christoph Bantz3Michael Maskos4Ronald E. Unger5C. James Kirkpatrick6Institute of Pathology, University Medical Center Mainz, Langenbeckstr. 1, 55101 Mainz, GermanyInstitute of Pathology, University Medical Center Mainz, Langenbeckstr. 1, 55101 Mainz, GermanyInstitute of Pathology, University Medical Center Mainz, Langenbeckstr. 1, 55101 Mainz, GermanyFraunhofer ICT-IMM, Carl-Zeiss-Str. 18–20, 55129 Mainz, GermanyFraunhofer ICT-IMM, Carl-Zeiss-Str. 18–20, 55129 Mainz, GermanyInstitute of Pathology, University Medical Center Mainz, Langenbeckstr. 1, 55101 Mainz, GermanyInstitute of Pathology, University Medical Center Mainz, Langenbeckstr. 1, 55101 Mainz, GermanyThe air–blood barrier is a very thin membrane of about 2.2 µm thickness and therefore represents an ideal portal of entry for nanoparticles to be used therapeutically in a regenerative medicine strategy. Until now, numerous studies using cellular airway models have been conducted in vitro in order to investigate the potential hazard of NPs. However, in most in vitro studies a crucial alveolar component has been neglected. Before aspirated NPs encounter the cellular air–blood barrier, they impinge on the alveolar surfactant layer (10–20 nm in thickness) that lines the entire alveolar surface. Thus, a prior interaction of NPs with pulmonary surfactant components will occur. In the present study we explored the impact of pulmonary surfactant on the cytotoxic potential of amorphous silica nanoparticles (aSNPs) using in vitro mono- and complex coculture models of the air–blood barrier. Furthermore, different surface functionalisations (plain-unmodified, amino, carboxylate) of the aSNPs were compared in order to study the impact of chemical surface properties on aSNP cytotoxicity in combination with lung surfactant. The alveolar epithelial cell line A549 was used in mono- and in coculture with the microvascular cell line ISO-HAS-1 in the form of different cytotoxicity assays (viability, membrane integrity, inflammatory responses such as IL-8 release). At a distinct concentration (100 µg/mL) aSNP–plain displayed the highest cytotoxicity and IL-8 release in monocultures of A549. aSNP–NH2 caused a slight toxic effect, whereas aSNP–COOH did not exhibit any cytotoxicity. In combination with lung surfactant, aSNP–plain revealed an increased cytotoxicity in monocultures of A549, aSNP–NH2 caused a slightly augmented toxic effect, whereas aSNP–COOH did not show any toxic alterations. A549 in coculture did not show any decreased toxicity (membrane integrity) for aSNP–plain in combination with lung surfactant. However, a significant augmented IL-8 release was observed, but no alterations in combination with lung surfactant. The augmented aSNP toxicity with surfactant in monocultures appears to depend on the chemical surface properties of the aSNPs. Reactive silanol groups seem to play a crucial role for an augmented toxicity of aSNPs. The A549 cells in the coculture seem to be more robust towards aSNPs, which might be a result of a higher differentiation and polarization state due the longer culture period.https://doi.org/10.3762/bjnano.6.54air–blood barriercytotoxicityinflammatory responsepulmonary surfactantsilica nanoparticles |
spellingShingle | Jennifer Y. Kasper Lisa Feiden Maria I. Hermanns Christoph Bantz Michael Maskos Ronald E. Unger C. James Kirkpatrick Pulmonary surfactant augments cytotoxicity of silica nanoparticles: Studies on an in vitro air–blood barrier model Beilstein Journal of Nanotechnology air–blood barrier cytotoxicity inflammatory response pulmonary surfactant silica nanoparticles |
title | Pulmonary surfactant augments cytotoxicity of silica nanoparticles: Studies on an in vitro air–blood barrier model |
title_full | Pulmonary surfactant augments cytotoxicity of silica nanoparticles: Studies on an in vitro air–blood barrier model |
title_fullStr | Pulmonary surfactant augments cytotoxicity of silica nanoparticles: Studies on an in vitro air–blood barrier model |
title_full_unstemmed | Pulmonary surfactant augments cytotoxicity of silica nanoparticles: Studies on an in vitro air–blood barrier model |
title_short | Pulmonary surfactant augments cytotoxicity of silica nanoparticles: Studies on an in vitro air–blood barrier model |
title_sort | pulmonary surfactant augments cytotoxicity of silica nanoparticles studies on an in vitro air blood barrier model |
topic | air–blood barrier cytotoxicity inflammatory response pulmonary surfactant silica nanoparticles |
url | https://doi.org/10.3762/bjnano.6.54 |
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