Silver nanowire interactions with primary human alveolar type-II epithelial cell secretions

Contrasting bioreactivity with human alveolar type-I and type-II epithelial cells

Sinbad Sweeney, Ioannis G. Theodorou, Marta Zambianchi, Shu Chen, Andrew Gow, Stephan Schwander, Junfeng Zhang, Kian Fan Chung, Milo S P Shaffer, Mary P. Ryan, Alexandra E. Porter, Teresa D. Tetley

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Inhaled nanoparticles have a high deposition rate in the alveolar units of the deep lung. The alveolar epithelium is composed of type-I and type-II epithelial cells (ATI and ATII respectively) and is bathed in pulmonary surfactant. The effect of native human ATII cell secretions on nanoparticle toxicity is not known. We investigated the cellular uptake and toxicity of silver nanowires (AgNWs; 70 nm diameter, 1.5 μm length) with human ATI-like cells (TT1), in the absence or presence of Curosurf® (a natural porcine pulmonary surfactant with a low amount of protein) or harvested primary human ATII cell secretions (HAS; containing both the complete lipid as well as the full protein complement of human pulmonary surfactant i.e. SP-A, SP-B, SP-C and SP-D). We hypothesised that Curosurf® or HAS would confer improved protection for TT1 cells, limiting the toxicity of AgNWs. In agreement with our hypothesis, HAS reduced the inflammatory and reactive oxygen species (ROS)-generating potential of AgNWs with exposed TT1 cells. For example, IL-8 release and ROS generation was reduced by 38% and 29%, respectively, resulting in similar levels to that of the non-treated controls. However in contrast to our hypothesis, Curosurf® had no effect. We found a significant reduction in AgNW uptake by TT1 cells in the presence of HAS but not Curosurf. Furthermore, we show that the SP-A and SP-D are likely to be involved in this process as they were found to be specifically bound to the AgNWs. While ATI cells appear to be protected by HAS, evidence suggested that ATII cells, despite no uptake, were vulnerable to AgNW exposure (indicated by increased IL-8 release and ROS generation and decreased intracellular SP-A levels one day post-exposure). This study provides unique findings that may be important for the study of lung epithelial-endothelial translocation of nanoparticles in general and associated toxicity within the alveolar unit.

Original languageEnglish
Pages (from-to)10398-10409
Number of pages12
JournalNanoscale
Volume7
Issue number23
DOIs
Publication statusPublished - 21 Jun 2015
Externally publishedYes

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Pulmonary Surfactants
Silver
Nanowires
Toxicity
Pulmonary Surfactant-Associated Protein D
Reactive Oxygen Species
Surface active agents
Nanoparticles
Interleukin-8
Oxygen
Proteins
Deposition rates
Lipids
Complement System Proteins
poractant alfa
Epithelial Cells

ASJC Scopus subject areas

  • Materials Science(all)

Cite this

Silver nanowire interactions with primary human alveolar type-II epithelial cell secretions : Contrasting bioreactivity with human alveolar type-I and type-II epithelial cells. / Sweeney, Sinbad; Theodorou, Ioannis G.; Zambianchi, Marta; Chen, Shu; Gow, Andrew; Schwander, Stephan; Zhang, Junfeng; Chung, Kian Fan; Shaffer, Milo S P; Ryan, Mary P.; Porter, Alexandra E.; Tetley, Teresa D.

In: Nanoscale, Vol. 7, No. 23, 21.06.2015, p. 10398-10409.

Research output: Contribution to journalArticle

Sweeney, S, Theodorou, IG, Zambianchi, M, Chen, S, Gow, A, Schwander, S, Zhang, J, Chung, KF, Shaffer, MSP, Ryan, MP, Porter, AE & Tetley, TD 2015, 'Silver nanowire interactions with primary human alveolar type-II epithelial cell secretions: Contrasting bioreactivity with human alveolar type-I and type-II epithelial cells', Nanoscale, vol. 7, no. 23, pp. 10398-10409. https://doi.org/10.1039/c5nr01496d
Sweeney, Sinbad ; Theodorou, Ioannis G. ; Zambianchi, Marta ; Chen, Shu ; Gow, Andrew ; Schwander, Stephan ; Zhang, Junfeng ; Chung, Kian Fan ; Shaffer, Milo S P ; Ryan, Mary P. ; Porter, Alexandra E. ; Tetley, Teresa D. / Silver nanowire interactions with primary human alveolar type-II epithelial cell secretions : Contrasting bioreactivity with human alveolar type-I and type-II epithelial cells. In: Nanoscale. 2015 ; Vol. 7, No. 23. pp. 10398-10409.
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abstract = "Inhaled nanoparticles have a high deposition rate in the alveolar units of the deep lung. The alveolar epithelium is composed of type-I and type-II epithelial cells (ATI and ATII respectively) and is bathed in pulmonary surfactant. The effect of native human ATII cell secretions on nanoparticle toxicity is not known. We investigated the cellular uptake and toxicity of silver nanowires (AgNWs; 70 nm diameter, 1.5 μm length) with human ATI-like cells (TT1), in the absence or presence of Curosurf{\circledR} (a natural porcine pulmonary surfactant with a low amount of protein) or harvested primary human ATII cell secretions (HAS; containing both the complete lipid as well as the full protein complement of human pulmonary surfactant i.e. SP-A, SP-B, SP-C and SP-D). We hypothesised that Curosurf{\circledR} or HAS would confer improved protection for TT1 cells, limiting the toxicity of AgNWs. In agreement with our hypothesis, HAS reduced the inflammatory and reactive oxygen species (ROS)-generating potential of AgNWs with exposed TT1 cells. For example, IL-8 release and ROS generation was reduced by 38{\%} and 29{\%}, respectively, resulting in similar levels to that of the non-treated controls. However in contrast to our hypothesis, Curosurf{\circledR} had no effect. We found a significant reduction in AgNW uptake by TT1 cells in the presence of HAS but not Curosurf. Furthermore, we show that the SP-A and SP-D are likely to be involved in this process as they were found to be specifically bound to the AgNWs. While ATI cells appear to be protected by HAS, evidence suggested that ATII cells, despite no uptake, were vulnerable to AgNW exposure (indicated by increased IL-8 release and ROS generation and decreased intracellular SP-A levels one day post-exposure). This study provides unique findings that may be important for the study of lung epithelial-endothelial translocation of nanoparticles in general and associated toxicity within the alveolar unit.",
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AU - Schwander, Stephan

AU - Zhang, Junfeng

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