Pulmonary Surfactant

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Yi Y. Zuo - One of the best experts on this subject based on the ideXlab platform.

  • Shape affects the interactions of nanoparticles with Pulmonary Surfactant
    Science China. Materials, 2015
    Co-Authors: Xubo Lin, Yi Y. Zuo
    Abstract:

    The interactions with the Pulmonary Surfactant, the initial biological barrier of respiratory pathway, determine the potential therapeutic applications and toxicological effects of inhaled nanoparticles (NPs). Although much attention has been paid to optimize the physicochemical properties of NPs for improved delivery and targeting, shape effects of the inhaled NPs on their interactions with the Pulmonary Surfactant are still far from clear. Here, we studied the shape effects of NPs on their penetration abilities and structural disruptions to the dipalmitoylphosphatidylcholine (DPPC) monolayer (being model Pulmonary Surfactant film) using coarse-grained molecular dynamics simulations. It is found that during the inspiration process (i.e., Surfactant film expansion), shape effects are negligible. However, during the expiration process (i.e., Surfactant film compression), NPs of different shapes show various penetration abilities and degrees of structural disruptions to the DPPC monolayer. We found that rod-like NPs showed the highest degree of penetration and the smallest side-effects to the DPPC monolayer. Our results may provide a useful insight into the design of NPs for respiratory therapeutics.

  • physicochemical properties of nanoparticles regulate translocation across Pulmonary Surfactant monolayer and formation of lipoprotein corona
    ACS Nano, 2013
    Co-Authors: Bao Jiao, Xinghua Shi, Russell P Valle, Qihui Fan, Yi Y. Zuo
    Abstract:

    Interaction with the Pulmonary Surfactant film, being the first line of host defense, represents the initial bio-nano interaction in the lungs. Such interaction determines the fate of the inhaled nanoparticles and their potential therapeutic or toxicological effect. Despite considerable progress in optimizing physicochemical properties of nanoparticles for improved delivery and targeting, the mechanisms by which inhaled nanoparticles interact with the Pulmonary Surfactant film are still largely unknown. Here, using combined in vitro and in silico methods, we show how hydrophobicity and surface charge of nanoparticles differentially regulate the translocation and interaction with the Pulmonary Surfactant film. While hydrophilic nanoparticles generally translocate quickly across the Pulmonary Surfactant film, a significant portion of hydrophobic nanoparticles are trapped by the Surfactant film and encapsulated in lipid protrusions upon film compression. Our results support a novel model of Pulmonary Surfactant lipoprotein corona associated with inhaled nanoparticles of different physicochemical properties. Our data suggest that the study of Pulmonary nanotoxicology and nanoparticle-based Pulmonary drug delivery should consider this lipoprotein corona.

  • adverse biophysical effects of hydroxyapatite nanoparticles on natural Pulmonary Surfactant
    ACS Nano, 2011
    Co-Authors: Qihui Fan, Yi E Wang, Xinxin Zhao, Joachim Say Chye Loo, Yi Y. Zuo
    Abstract:

    Inhaled nanoparticles (NPs) must first interact with the Pulmonary Surfactant (PS) lining layer that covers the entire internal surface of the respiratory tract and plays an important role in surfa...

Nils O Petersen - One of the best experts on this subject based on the ideXlab platform.

  • metal nanoparticle pollutants interfere with Pulmonary Surfactant function in vitro
    Biophysical Journal, 2008
    Co-Authors: Mandeep Singh Bakshi, Lin Zhao, Ronald Smith, Fred Possmayer, Nils O Petersen
    Abstract:

    Reported associations between air pollution and Pulmonary and cardiovascular diseases prompted studies on the effects of gold nanoparticles (Au NP) on Pulmonary Surfactant function. Low levels (3.7 mol % Au/lipid, 0.98% wt/wt) markedly inhibited adsorption of a semisynthetic Pulmonary Surfactant (dipalmitoyl-phosphatidylcholine (DPPC)/palmitoyl-oleoyl-phosphatidylglycerol/Surfactant protein B (SP-B); 70:30:1 wt %). Au NP also impeded the Surfactant's ability to reduce surface tension (γ) to low levels during film compression and to respread during film expansion. Transmission electron microscopy showed that Au NP generated by a seed-growth method were spherical with diameters of ∼15 nm. Including palmitoyl-oleoyl-phosphatidylglycerol appeared to coat the NP with at least one lipid bilayer but did not affect NP shape or size. Similar overall observations occurred with dimyristoyl phosphatidylglycerol. Dipalmitoyl-phosphatidylglycerol was less effective in NP capping, although similar sized NP were formed. Including SP-B (1% wt/wt) appears to induce the formation of elongated strands of interacting threads with the fluid phosphatidylglycerols (PG). Including DPPC resulted in formation of aggregated, less spherical NP with a larger size distribution. With DPPC, strand formation due to SP-B was not observed. Agarose gel electrophoresis studies demonstrated that the aggregation induced by SP-B blocked migration of PG-coated NP. Migration was also influenced by the fluidity of the PGs. It is concluded that Au NP can interact with and sequester Pulmonary Surfactant phospholipids and, if inhaled from the atmosphere, could impede Pulmonary Surfactant function in the lung.

Alan H Jobe - One of the best experts on this subject based on the ideXlab platform.

  • Pulmonary Surfactant therapy
    The New England Journal of Medicine, 1993
    Co-Authors: Alan H Jobe
    Abstract:

    In 1959, not long after Surfactant had been identified as critical to maintaining lung inflation at low transPulmonary pressures,1,2 Avery and Mead3 reported that saline extracts from the lungs of preterm infants with respiratory distress syndrome lacked the low surface tension characteristic of Pulmonary Surfactant. After several unsuccessful attempts to treat infants with respiratory distress syndrome with aerosolized Surfactant,4,5 intratracheal administration of Surfactant recovered from the air spaces of mature animal lungs was found to improve lung expansion and ventilation in preterm animals6–8. The clinical potential of Surfactant treatment for respiratory distress syndrome was demonstrated by . . .

Fred Possmayer - One of the best experts on this subject based on the ideXlab platform.

  • metal nanoparticle pollutants interfere with Pulmonary Surfactant function in vitro
    Biophysical Journal, 2008
    Co-Authors: Mandeep Singh Bakshi, Lin Zhao, Ronald Smith, Fred Possmayer, Nils O Petersen
    Abstract:

    Reported associations between air pollution and Pulmonary and cardiovascular diseases prompted studies on the effects of gold nanoparticles (Au NP) on Pulmonary Surfactant function. Low levels (3.7 mol % Au/lipid, 0.98% wt/wt) markedly inhibited adsorption of a semisynthetic Pulmonary Surfactant (dipalmitoyl-phosphatidylcholine (DPPC)/palmitoyl-oleoyl-phosphatidylglycerol/Surfactant protein B (SP-B); 70:30:1 wt %). Au NP also impeded the Surfactant's ability to reduce surface tension (γ) to low levels during film compression and to respread during film expansion. Transmission electron microscopy showed that Au NP generated by a seed-growth method were spherical with diameters of ∼15 nm. Including palmitoyl-oleoyl-phosphatidylglycerol appeared to coat the NP with at least one lipid bilayer but did not affect NP shape or size. Similar overall observations occurred with dimyristoyl phosphatidylglycerol. Dipalmitoyl-phosphatidylglycerol was less effective in NP capping, although similar sized NP were formed. Including SP-B (1% wt/wt) appears to induce the formation of elongated strands of interacting threads with the fluid phosphatidylglycerols (PG). Including DPPC resulted in formation of aggregated, less spherical NP with a larger size distribution. With DPPC, strand formation due to SP-B was not observed. Agarose gel electrophoresis studies demonstrated that the aggregation induced by SP-B blocked migration of PG-coated NP. Migration was also influenced by the fluidity of the PGs. It is concluded that Au NP can interact with and sequester Pulmonary Surfactant phospholipids and, if inhaled from the atmosphere, could impede Pulmonary Surfactant function in the lung.

  • the role of lipids in Pulmonary Surfactant
    Biochimica et Biophysica Acta, 1998
    Co-Authors: Ruud A. W. Veldhuizen, Sandra Orgeig, Kaushik Nag, Fred Possmayer
    Abstract:

    Pulmonary Surfactant is composed of approx. 90% lipids and 10% protein. This review article focusses on the lipid components of Surfactant. The first sections will describe the lipid composition of mammalian Surfactant and the techniques that have been utilized to study the involvement of these lipids in reducing the surface tension at an air-liquid interface, the main function of Pulmonary Surfactant. Subsequently, the roles of specific lipids in Surfactant will be discussed. For the two main Surfactant phospholipids, phosphatidylcholine and phosphatidylglycerol, specific contributions to the overall surface tension reducing properties of Surfactant have been indicated. In contrast, the role of the minor phospholipid components and the neutral lipid fraction of Surfactant is less clear and requires further study. Recent technical advances, such as fluorescent microscopic techniques, hold great potential for expanding our knowledge of how Surfactant lipids, including some of the minor components, function. Interesting information regarding Surfactant lipids has also been obtained in studies evaluating the Surfactant system in non-mammalian species. In certain non-mammalian species (and at least one marsupial), Surfactant lipid composition, most notably disaturated phosphatidylcholine and cholesterol, changes drastically under different conditions such as an alteration in body temperature. The impact of these changes on Surfactant function provide insight into the function of these lipids, not only in non-mammalian lungs but also in the Surfactant from mammalian species.

Bao Jiao - One of the best experts on this subject based on the ideXlab platform.

  • physicochemical properties of nanoparticles regulate translocation across Pulmonary Surfactant monolayer and formation of lipoprotein corona
    ACS Nano, 2013
    Co-Authors: Bao Jiao, Xinghua Shi, Russell P Valle, Qihui Fan, Yi Y. Zuo
    Abstract:

    Interaction with the Pulmonary Surfactant film, being the first line of host defense, represents the initial bio-nano interaction in the lungs. Such interaction determines the fate of the inhaled nanoparticles and their potential therapeutic or toxicological effect. Despite considerable progress in optimizing physicochemical properties of nanoparticles for improved delivery and targeting, the mechanisms by which inhaled nanoparticles interact with the Pulmonary Surfactant film are still largely unknown. Here, using combined in vitro and in silico methods, we show how hydrophobicity and surface charge of nanoparticles differentially regulate the translocation and interaction with the Pulmonary Surfactant film. While hydrophilic nanoparticles generally translocate quickly across the Pulmonary Surfactant film, a significant portion of hydrophobic nanoparticles are trapped by the Surfactant film and encapsulated in lipid protrusions upon film compression. Our results support a novel model of Pulmonary Surfactant lipoprotein corona associated with inhaled nanoparticles of different physicochemical properties. Our data suggest that the study of Pulmonary nanotoxicology and nanoparticle-based Pulmonary drug delivery should consider this lipoprotein corona.