Physicochemical Properties of Nanoparticles Regulate Translocation across Pulmonary Surfactant Monolayer and Formation of Lipoprotein Corona

Hu, Guoqing; Jiao, Bao Xiang; Shi, Xinghua; Valle, Russell P.; Fan, Qihui; Zuo, Yi Y.

doi:10.1021/nn4054683

Cited by 185 publications

(223 citation statements)

References 56 publications

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“…This is in agreement with previous experimental studies. 19,54 When the area per molecule was increased to 0.64 and 0.68 nm 2 , pore formation was observed (Fig. 2), indicating the coexistence between the LE phase and a 2D gas phase.…”

Section: Resultsmentioning

confidence: 97%

Lipid monolayer disruption caused by aggregated carbon nanoparticles

et al. 2015

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Carbon nanoparticles (CNP) have significant impact on the Pulmonary Surfactant (PS), the first biological barrier in the respiratory system. CNPs -abundant in the environment due to combustion -can translocate into our bodies by crossing the alveolar epithelium barrier, and they can be retained in the lungs due to slow clearance. The physical mechanisms of how CNPs perturb PS remain unclear yet such knowledge is crucial for developing effective strategies against the adverse effects of CNPs. Molecular dynamics (MD) simulations of model PS monolayers in the presence of C 60 fullerenes were performed at time scales of tens of microseconds and varying C 60 content. In contrast to bilayers, fullerenes affected both structural and dynamic properties of the PS monolayer. Surface tension/area isotherms of the monolayer were changed by fullerenes and perturbations of the physical structure of the PS monolayer became major at high fullerene concentrations due to fullerene aggregation. At high compression (area per molecule of 0.48 nm 2 ), the monolayer became unstable and collapsed forming a bilayer in the water phase. At low compression, pore formation occurred. Free energy calculations suggest that increasing fullerene concentration leads to decreased preference for the fullerenes to reside inside the monolayer.However, the free energy barrier for transferring fullerene out of the monolayer is rather large at all fullerene concentrations; spontaneous translocation of fullerene out of the monolayer is thermodynamically unfavorable. The results illustrate some of the potentially harmful effects of CNPs on the respiratory system and also the physical mechanism of how CNPs disturb pulmonary surfactant. This may be related to the difficulty of CNP clearance from lung surfactant. The total simulation time was 370 microseconds.

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Section: Resultsmentioning

confidence: 97%

Lipid monolayer disruption caused by aggregated carbon nanoparticles

et al. 2015

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“…16,26 Consequently, the hydrophobic NPs are expected to have a higher inhibitory potential to the biophysical function of natural PS than the hydrophilic NPs. Along this line, our in vitro experiments showed that NPs with increasing hydrophobicity cause a higher degree of surfactant inhibition, likely due to depletion of hydrophobic proteins from the natural PS.…”

Section: Resultsmentioning

confidence: 99%

Unveiling the Molecular Structure of Pulmonary Surfactant Corona on Nanoparticles

et al. 2017

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The growing risk of human exposure to airborne nanoparticles (NPs) causes a general concern on the biosafety of nanotechnology. Inhaled NPs can deposit in the deep lung at which they interact with the pulmonary surfactant (PS). Despite the increasing study of nano-bio interactions, detailed molecular mechanisms by which inhaled NPs interact with the natural PS system remain unclear. Using coarse-grained molecular dynamics simulation, we studied the interaction between NPs and the PS system in the alveolar fluid. It was found that regardless of different physicochemical properties, upon contacting the PS, both silver and polystyrene NPs are immediately coated with a biomolecular corona that consists of both lipids and proteins. Structure and molecular conformation of the PS corona depend on the hydrophobicity of the pristine NPs. Quantitative analysis revealed that lipid composition of the corona formed on different NPs is relatively conserved and is similar to that of the bulk phase PS. However, relative abundance of the surfactant-associated proteins, SP-A, SP-B, and SP-C, is notably affected by the hydrophobicity of the NP. The PS corona provides the NPs with a physicochemical barrier against the environment, equalizes the hydrophobicity of the pristine NPs, and may enhance biorecognition of the NPs. These modifications in physicochemical properties may play a crucial role in affecting the biological identity of the NPs and hence alter their subsequent interactions with cells and other biological entities. Our results suggest that all studies of inhalation nanotoxicology or NP-based pulmonary drug delivery should consider the influence of the PS corona.

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“…These NP handling techniques are largely limited by the in vitro experimental methodologies used in previous studies, including the Langmuir trough, 10–14 pulsating bubble surfactometer (PBS), 15–17 and captive bubble surfactometer (CBS). 18,19 Figure 1 shows the schematics of the Langmuir trough, PBS, 21 and CBS 22 for studying NP–PS interactions.…”

mentioning

confidence: 99%

Biophysical Influence of Airborne Carbon Nanomaterials on Natural Pulmonary Surfactant

2015

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Inhalation of nanoparticles (NP), including lightweight airborne carbonaceous nanomaterials (CNM), poses a direct and systemic health threat to those who handle them. Inhaled NP penetrate deep pulmonary structures in which they first interact with the pulmonary surfactant (PS) lining at the alveolar air–water interface. In spite of many research efforts, there is a gap of knowledge between in vitro biophysical study and in vivo inhalation toxicology since all existing biophysical models handle NP–PS interactions in the liquid phase. This technical limitation, inherent in current in vitro methodologies, makes it impossible to simulate how airborne NP deposit at the PS film and interact with it. Existing in vitro NP–PS studies using liquid-suspended particles have been shown to artificially inflate the no-observed adverse effect level of NP exposure when compared to in vivo inhalation studies and international occupational exposure limits (OELs). Here, we developed an in vitro methodology called the constrained drop surfactometer (CDS) to quantitatively study PS inhibition by airborne CNM. We show that airborne multiwalled carbon nanotubes and graphene nanoplatelets induce a concentration-dependent PS inhibition under physiologically relevant conditions. The CNM aerosol concentrations controlled in the CDS are comparable to those defined in international OELs. Development of the CDS has the potential to advance our understanding of how submicron airborne nanomaterials affect the PS lining of the lung.

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Physicochemical Properties of Nanoparticles Regulate Translocation across Pulmonary Surfactant Monolayer and Formation of Lipoprotein Corona

Cited by 185 publications

References 56 publications

Lipid monolayer disruption caused by aggregated carbon nanoparticles

Lipid monolayer disruption caused by aggregated carbon nanoparticles

Unveiling the Molecular Structure of Pulmonary Surfactant Corona on Nanoparticles

Biophysical Influence of Airborne Carbon Nanomaterials on Natural Pulmonary Surfactant

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