Effect of pulmonary surfactant on the dissolution, stability and uptake of zinc oxide nanowires by human respiratory epithelial cells

Theodorou, Ioannis G.; Ruenraroengsak, Pakatip; Gow, Andrew J.; Schwander, Stephan; Zhang, Junfeng Jim; Chung, Kian Fan; Tetley, Teresa D.; Ryan, Mary P.; Porter, Alexandra E.

doi:10.1080/17435390.2016.1214762

Cited by 43 publications

(25 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As our studies are performed on the short‐term exposure (24 h) of cells to NPs, this does not resemble the in vivo situation, where upon peritumoral administration of the NPs, the cancer cells will be exposed to the NPs for longer time periods. The 24 h exposure time has been chosen in line with literature, where cellular NP exposure is often 24 h, mainly driven by the fact that for efficient cellular NP uptake, cells should have undergone one cell cycle . As for different cell types, the cell cycle duration can differ quite a bit, a time period of 24 h is chosen as a mean value.…”

Section: Resultsmentioning

confidence: 99%

Presence of an Immune System Increases Anti‐Tumor Effect of Ag Nanoparticle Treated Mice

Manshian

Jiménez

Himmelreich

et al. 2016

Adv Healthcare Materials

View full text Add to dashboard Cite

To date, most nanomedical studies rely on the use of immune-deficient mice in which the contribution of the immune system on the applied therapy is ignored. Here, the degradation of silver nanoparticles (Ag NPs) is exploited as a means to treat subcutaneous tumor models in mice. To investigate the impact of the immune system, the same tumor cell type (KLN 205 murine squamous cell carcinoma) is used in a xenograft model in NOD SCIDγ immune-deficient mice and as a syngeneic model in immune-competent DBA/2 mice. The Ag NPs are screened for their cytotoxicity on various cancer cell lines, indicating a concentration-dependent induction of oxidative stress, mitochondrial damage, and autophagy on all cell types tested. At subcytotoxic concentrations, prolonged cellular exposure to the Ag NPs results in toxicity due to NP degradation and the generation of toxic Ag ions. At subcytotoxic conditions, the NPs are found to cause inflammation in vitro. Similar results are obtained in the immune-competent mouse model, where clear inflammation is observed after treatment of the implanted tumors with Ag NPs. This inflammation leads to an ongoing antitumoral effect, which results in a significantly reduced tumor growth compared to Ag NP-treated tumors in an immune-deficient model.

show abstract

Section: Resultsmentioning

confidence: 99%

Presence of an Immune System Increases Anti‐Tumor Effect of Ag Nanoparticle Treated Mice

Manshian

Jiménez

Himmelreich

et al. 2016

Adv Healthcare Materials

View full text Add to dashboard Cite

show abstract

“…For example, corona layer was found to impair nanoparticle adhesion onto cell surface or to decrease particle uptake by macrophages [16,28,29]. On the other hand, some studies reported an improved cell internalization [14,30,31,32]. Therefore, the implications of corona layer on AM targeting using inhalable carriers remain still an open issue that needs to be further explored.…”

Section: Introductionmentioning

confidence: 99%

The Impact of Lipid Corona on Rifampicin Intramacrophagic Transport Using Inhaled Solid Lipid Nanoparticles Surface-Decorated with a Mannosylated Surfactant

et al. 2019

View full text Add to dashboard Cite

The mimicking of physiological conditions is crucial for the success of accurate in vitro studies. For inhaled nanoparticles, which are designed for being deposited on alveolar epithelium and taken up by macrophages, it is relevant to investigate the interactions with pulmonary surfactant lining alveoli. As a matter of fact, the formation of a lipid corona layer around the nanoparticles could modulate the cell internalization and the fate of the transported drugs. Based on this concept, the present research focused on the interactions between pulmonary surfactant and Solid Lipid Nanoparticle assemblies (SLNas), loaded with rifampicin, an anti-tuberculosis drug. SLNas were functionalized with a synthesized mannosylated surfactant, both alone and in a blend with sodium taurocholate, to achieve an active targeting to mannose receptors present on alveolar macrophages (AM). Physico-chemical properties of the mannosylated SLNas satisfied the requirements relative to suitable respirability, drug payload, and AM active targeting. Our studies have shown that a lipid corona is formed around SLNas in the presence of Curosurf, a commercial substitute of the natural pulmonary surfactant. The lipid corona promoted an additional resistance to the drug diffusion for SLNas functionalized with the mannosylated surfactant and this improved drug retention within SLNas before AM phagocytosis takes place. Moreover, lipid corona formation did not modify the role of nanoparticle mannosylation towards the specific receptors on MH-S cell membrane.

show abstract

“…5e and f, pre-incubation with Infasurf remarkably reduced MCN-induced toxicity, as reflected by elevated cell viability and improved cellular morphology relative to treated cells without surfactant pre-incubation (p < 0.05). It indicates that the pulmonary surfactant corona formed on the surface of MCNs effectively reduced cytotoxicity of this nanomaterial, similar to the effect of surfactant made on silver nanoparticles (Sweeney et al, 2016;Theodorou et al, 2016).…”

Section: L-mcns Induced More Cytotoxicity Than I-mcns and S-mcnsmentioning

confidence: 57%

Mesoporous carbon nanomaterials induced pulmonary surfactant inhibition, cytotoxicity, inflammation and lung fibrosis

Chen

Yang

et al. 2017

Journal of Environmental Sciences

View full text Add to dashboard Cite

Environmental exposure and health risk upon engineered nanomaterials are increasingly concerned. The family of mesoporous carbon nanomaterials (MCNs) is a rising star in nanotechnology for multidisciplinary research with versatile applications in electronics, energy and gas storage, and biomedicine. Meanwhile, there is mounting concern on their environmental health risks due to the growing production and usage of MCNs. The lung is the primary site for particle invasion under environmental exposure to nanomaterials. Here, we studied the comprehensive toxicological profile of MCNs in the lung under the scenario of moderate environmental exposure. It was found that at a low concentration of 10μg/mL MCNs induced biophysical inhibition of natural pulmonary surfactant. Moreover, MCNs at similar concentrations reduced viability of J774A.1 macrophages and lung epithelial A549 cells. Incubating with nature pulmonary surfactant effectively reduced the cytotoxicity of MCNs. Regarding the pro-inflammatory responses, MCNs activated macrophages in vitro, and stimulated lung inflammation in mice after inhalation exposure, associated with lung fibrosis. Moreover, we found that the size of MCNs played a significant role in regulating cytotoxicity and pro-inflammatory potential of this nanomaterial. In general, larger MCNs induced more pronounced cytotoxic and pro-inflammatory effects than their smaller counterparts. Our results provided valuable information on the toxicological profile and environmental health risks of MCNs, and suggested that fine-tuning the size of MCNs could be a practical precautionary design strategy to increase safety and biocompatibility of this nanomaterial.

show abstract

Effect of pulmonary surfactant on the dissolution, stability and uptake of zinc oxide nanowires by human respiratory epithelial cells

Cited by 43 publications

References 49 publications

Presence of an Immune System Increases Anti‐Tumor Effect of Ag Nanoparticle Treated Mice

Presence of an Immune System Increases Anti‐Tumor Effect of Ag Nanoparticle Treated Mice

The Impact of Lipid Corona on Rifampicin Intramacrophagic Transport Using Inhaled Solid Lipid Nanoparticles Surface-Decorated with a Mannosylated Surfactant

Mesoporous carbon nanomaterials induced pulmonary surfactant inhibition, cytotoxicity, inflammation and lung fibrosis

Contact Info

Product

Resources

About