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Journal articles on the topic 'Surfactant/Lipids'

Author: Grafiati

Published: 7 September 2023

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1

SHIMIZU, Takao. "Biologically Active Lipids: From Prostaglandins to Surfactant Lipids." Journal of the Mass Spectrometry Society of Japan 57, no. 3 (2009): 153–55. http://dx.doi.org/10.5702/massspec.57.153.

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2

Wright, J. R. "Clearance and recycling of pulmonary surfactant." American Journal of Physiology-Lung Cellular and Molecular Physiology 259, no. 2 (1990): L1—L12. http://dx.doi.org/10.1152/ajplung.1990.259.2.l1.

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In a steady state the rate of secretion of pulmonary surfactant lipids and proteins into the alveolar airspace must be balanced by the rate of removal. Several potential pathways for clearance have been identified including uptake by alveolar type II cells, which also synthesize and secrete surfactant components, uptake by other epithelial cells, and internalization by alveolar macrophages. A small amount of surfactant moves up the airways and through the epithelium-endothelium barrier into the blood. Some of the surfactant lipids and proteins that are cleared from the alveolar airspace appear

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3

KEOUGH, KEVIN M. W. "Physicochemical properties of surfactant lipids." Biochemical Society Transactions 13, no. 6 (1985): 1081–84. http://dx.doi.org/10.1042/bst0131081.

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4

Batenburg, J. J. "Surfactant phospholipids: synthesis and storage." American Journal of Physiology-Lung Cellular and Molecular Physiology 262, no. 4 (1992): L367—L385. http://dx.doi.org/10.1152/ajplung.1992.262.4.l367.

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Pulmonary surfactant, a complex consisting of 90% lipids and 10% specific proteins, lines the alveoli of the lung and prevents alveolar collapse and transudation by lowering the surface tension at the air-liquid interface. Dipalmitoylphosphatidylcholine constitutes approximately 50% of the surfactant lipids and is primarily responsible for the surface tension-lowering property of the surfactant mixture. This phospholipid, together with the other surfactant phospholipids, is produced at the endoplasmic reticulum of the alveolar type II epithelial cells. The characteristic lamellar bodies in the

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5

Casals, Cristina, Belen García-Fojeda, Paula Tenreiro, and Carlos M. Minutti. "Surfactant lipids inhibit PI3K-dependent signaling pathways induced by IL-4 in alveolar macrophages." Journal of Immunology 210, no. 1_Supplement (2023): 72.32. http://dx.doi.org/10.4049/jimmunol.210.supp.72.32.

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Abstract Alveolar macrophages (AMs) are less able to respond to IL-4 in vivo than macrophages from the peritoneal cavity, due to a still-unknown factor of the lung environment. The aim of this study is to investigate whether surfactant lipids, which are continuously endocytosed by AMs, could influence IL-4-mediated alternative activation and proliferation of AMs. To that end, AMs were preincubated with surfactant lipids and stimulated with IL-4 in the presence or absence of surfactant protein SP-A, an amplifier of IL-4 actions. We found that alveolar lipids reduced IL-4- and IL-4+SP-A-dependen

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6

Mudgil, Poonam, and Thomas J. Millar. "Surfactant Properties of Human Meibomian Lipids." Investigative Opthalmology & Visual Science 52, no. 3 (2011): 1661. http://dx.doi.org/10.1167/iovs.10-5445.

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7

Van Iwaarden, J. F., H. Shimizu, P. H. M. Van Golde, D. R. Voelker, and L. M. G. Van Golde. "Rat surfactant protein D enhances the production of oxygen radicals by rat alveolar macrophages." Biochemical Journal 286, no. 1 (1992): 5–8. http://dx.doi.org/10.1042/bj2860005.

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Rat surfactant protein D (SP-D) was shown to enhance the production of oxygen radicals by rat alveolar macrophages. This enhancement, which was determined by a lucigenin-dependent chemiluminescence assay, was maximal after 18 min at an SP-D concentration of 0.2 micrograms/ml. Surfactant lipids did not influence the stimulation of alveolar macrophages by SP-D, whereas the oxygen-radical production of these cells induced by surfactant protein A was inhibited by the lipids in a concentration-dependent manner.

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8

Kremlev, S. G., and D. S. Phelps. "Effect of SP-A and surfactant lipids on expression of cell surface markers in the THP-1 monocytic cell line." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 6 (1997): L1070—L1077. http://dx.doi.org/10.1152/ajplung.1997.272.6.l1070.

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Pulmonary surfactant and its lipid components inhibit cell proliferation and cytokine expression. Surfactant protein A (SP-A) can stimulate these same functions. We assessed the impact of SP-A and surfactant lipids on the expression of the cell surface markers, CD14, CD54 (intercellular adhesion molecule-1), and CD11b, by the human monocytic cell line THP-1 using fluorescent antibody staining and fluorescence-activated cell sorting. Under basal conditions CD14 and CD54 were undetectable, and CD11b was expressed at low levels. Incubation of the cells in 1,25(OH)2D3 alone, or with low doses of s

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9

Soll, Roger F., and Jerold F. Lucey. "Surfactant Replacement Therapy." Pediatrics In Review 12, no. 9 (1991): 261–67. http://dx.doi.org/10.1542/pir.12.9.261.

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Despite medical and technological advances, respiratory distress syndrome (RDS) remains a major cause of morbidity and mortality in premature infants. Thirty years have passed since Avery and Mead demonstrated that infants dying of RDS were deficient in pulmonary surfactant. In those three decades, advances in our understanding of the composition, function, and metabolism of pulmonary surfactant have finally led to clinical trials of surfactant replacement therapy in thousands of premature infants. This article reviews the current status of surfactant replacement therapy. BACKGROUND Pulmonary

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10

Kremlev, S. G., T. M. Umstead, and D. S. Phelps. "Surfactant protein A regulates cytokine production in the monocytic cell line THP-1." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 5 (1997): L996—L1004. http://dx.doi.org/10.1152/ajplung.1997.272.5.l996.

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Surfactant lipids inhibit cytokine production by immune cells, and surfactant protein A (SP-A) stimulates it. By enzyme-linked immunosorbent assay and mRNA blotting, we studied proinflammatory cytokine production by the monocytic cell line THP-1. SP-A caused increases in tumor necrosis factor (TNF)-alpha within 1 h, peaking at 4 h and then declining. Interleukin (IL)-1 beta increased and stayed elevated for 24 h. SP-A stimulated IL-8 also, peaking at 4 h, rapidly declining, and peaking again at 24 h. SP-A-dependent changes were detected for IL-6, but at higher SP-A doses. mRNA levels for TNF-a

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11

Johnston, Sonya D., Christopher B. Daniels, David Cenzato, Jeffrey A. Whitsett, and Sandra Orgeig. "The pulmonary surfactant system matures upon pipping in the freshwater turtle Chelydra serpentina." Journal of Experimental Biology 205, no. 3 (2002): 415–25. http://dx.doi.org/10.1242/jeb.205.3.415.

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SUMMARY Pulmonary surfactant (PS), a mixture of phospholipids (PL), neutral lipids and surfactant proteins (SP), lowers surface tension within the lung, which increases lung compliance and improves the removal of fluid at birth. Here, we have examined the expression of thyroid transcription factor-1 (TTF-1) and the surfactant protein SP-B, and also the composition of pulmonary surfactant lipids in the developing lung of the turtle Chelydra serpentina. Lavage and lung tissue were collected from late embryonic, pipped and hatchling turtles. TTF-1, a regulator of gene expression of surfactant pro

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12

Young, S. L., and R. Silbajoris. "Dexamethasone increases adult rat lung surfactant lipids." Journal of Applied Physiology 60, no. 5 (1986): 1665–72. http://dx.doi.org/10.1152/jappl.1986.60.5.1665.

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Prenatal administration of glucocorticoids stimulates epithelial cell maturation and induces a precocious development of pulmonary surfactant. The response of the adult lung to steroid administration is less well understood. We administered dexamethasone (2 mg X kg-1 X day-1) to adult male rats for 1 wk by daily subcutaneous injection. After pentobarbital anesthesia we lavaged the lungs and also isolated lamellar bodies from the tissue. Lipid analyses of the extracellular and intracellular surfactant compartments showed two- to fourfold greater amounts of total phospholipids and disaturated ph

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13

Veldhuizen, Ruud, Kaushik Nag, Sandra Orgeig, and Fred Possmayer. "The role of lipids in pulmonary surfactant." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1408, no. 2-3 (1998): 90–108. http://dx.doi.org/10.1016/s0925-4439(98)00061-1.

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14

Polańska, Żaneta, Zuzanna Pietralik-Molińska, Daria Wojciechowska, et al. "The Process of Binding and Releasing of Genetic Material from Lipoplexes Based on Trimeric Surfactants and Phospholipids." International Journal of Molecular Sciences 22, no. 14 (2021): 7744. http://dx.doi.org/10.3390/ijms22147744.

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Nonviral vectors for gene therapy such as lipoplexes are characterized by low toxicity, high biocompatibility, and good transfection efficiency. Specifically, lipoplexes based on polymeric surfactants and phospholipids have great potential as gene carriers due to the increased ability to bind genetic material (multiplied positive electric charge) while lowering undesirable effects (the presence of lipids makes the system more like natural membranes). This study aimed to test the ability to bind and release genetic material by lipoplexes based on trimeric surfactants and lipid formulations of d

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15

Holm, B. A., and R. H. Notter. "Effects of hemoglobin and cell membrane lipids on pulmonary surfactant activity." Journal of Applied Physiology 63, no. 4 (1987): 1434–42. http://dx.doi.org/10.1152/jappl.1987.63.4.1434.

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These experiments characterize the effects of hemoglobin and erythrocyte membrane lipids on the dynamic surface activity and adsorption facility of whole lung surfactant (LS) and a calf lung surfactant extract (CLSE) used clinically in surfactant replacement therapy for the neonatal respiratory distress syndrome (RDS). The results show that, at concentrations from 25 to 200 mg/ml, hemoglobin (Hb) increased the minimum dynamic surface tension of LS or CLSE mixtures (0.5 and 1.0 mumol/ml) from less than 1 to 25 dyn/cm on an oscillating bubble apparatus at 37 degrees C. Similarly, erythrocyte mem

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16

Kobayashi, T., W. Z. Li, K. Tashiro, et al. "Disparity between tidal and static volumes of immature lungs treated with reconstituted surfactants." Journal of Applied Physiology 80, no. 1 (1996): 62–68. http://dx.doi.org/10.1152/jappl.1996.80.1.62.

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We biologically assessed functions of several reconstituted surfactants with the same minimum surface tension (2-3 mN/m) as “complete” porcine pulmonary surfactant (natural surfactant) but with longer surface adsorption times. Administration of natural surfactant (adsorption time 0.29 s) into the lungs of surfactant-deficient immature rabbits brought a tidal volume of 16.1 +/- 4.4 (SD) ml/kg during mechanical ventilation with 40 breaths/min and 20 cmH2O insufflation pressure. In static pressure-volume recordings, these animals showed a lung volume of 62.4 +/- 9.7 ml/kg at 30 cmH2O airway press

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17

Walther, Frans J., Monik Gupta, Larry M. Gordon, and Alan J. Waring. "An oxidation-resistant peptide mimic of surfactant protein B (B-YL) forms an amphipathic helix-hairpin in liposomes with high surface activity." Gates Open Research 2 (February 26, 2018): 13. http://dx.doi.org/10.12688/gatesopenres.12799.1.

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Background: Animal-derived surfactants containing surfactant proteins B (SP-B) and C (SP-C) are used to treat respiratory distress syndrome (RDS) in preterm infants. SP-B (79 residues) plays a pivotal role in lung function and the design of synthetic lung surfactant. Super Mini-B (SMB), a 41-residue peptide based on the N- and C-domains of SP-B joined with a turn and two disulfides, folds as an α-helix hairpin mimicking the properties of these domains in SP-B. Here, we studied ‘B-YL’, a 41-residue oxidation-resistant SMB variant that has its four Cys and two Met residues replaced by Tyr and Le

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18

Walther, Frans J., Monik Gupta, Larry M. Gordon, and Alan J. Waring. "A sulfur-free peptide mimic of surfactant protein B (B-YL) exhibits high in vitro and in vivo surface activities." Gates Open Research 2 (July 10, 2018): 13. http://dx.doi.org/10.12688/gatesopenres.12799.2.

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Background: Animal-derived surfactants containing surfactant proteins B (SP-B) and C (SP-C) are used to treat respiratory distress syndrome (RDS) in preterm infants. SP-B (79 residues) plays a pivotal role in lung function and the design of synthetic lung surfactant. Super Mini-B (SMB), a 41-residue peptide based on the N- and C-domains of SP-B covalently joined with a turn and two disulfides, folds as an α-helix hairpin mimicking the properties of these domains in SP-B. Here, we studied ‘B-YL’, a 41-residue SMB variant that has its four cysteine and two methionine residues replaced by tyrosin

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19

Frey, Shelli L., Luka Pocivavsek, Alan J. Waring, et al. "Functional importance of the NH2-terminal insertion sequence of lung surfactant protein B." American Journal of Physiology-Lung Cellular and Molecular Physiology 298, no. 3 (2010): L335—L347. http://dx.doi.org/10.1152/ajplung.00190.2009.

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Lung surfactant protein B (SP-B) is required for proper surface activity of pulmonary surfactant. In model lung surfactant lipid systems composed of saturated and unsaturated lipids, the unsaturated lipids are removed from the film at high compression. It is thought that SP-B helps anchor these lipids closely to the monolayer in three-dimensional cylindrical structures termed “nanosilos” seen by atomic force microscopy imaging of deposited monolayers at high surface pressures. Here we explore the role of the SP-B NH2 terminus in the formation and stability of these cylindrical structures, spec

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20

Wright, J. R., and D. C. Youmans. "Degradation of surfactant lipids and surfactant protein A by alveolar macrophages in vitro." American Journal of Physiology-Lung Cellular and Molecular Physiology 268, no. 5 (1995): L772—L780. http://dx.doi.org/10.1152/ajplung.1995.268.5.l772.

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Pulmonary surfactant is synthesized and secreted into the airspaces by the alveolar type II cell. After it is secreted, surfactant undergoes a series of poorly understood transformations resulting in formation of a surface tension-reducing surface at the air-liquid interface. The by-products of the surface film and/or other products of surfactant metabolism are eventually cleared from the alveolar space. Both the alveolar type II cell and the macrophage are thought to be involved in surfactant clearance and have been shown to internalize surfactant lipid in vitro. The goal of the current inves

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21

Thakur, N. R., M. Tesan, N. E. Tyler, and J. E. Bleasdale. "Altered lipid synthesis in type II pneumonocytes exposed to lung surfactant." Biochemical Journal 240, no. 3 (1986): 679–90. http://dx.doi.org/10.1042/bj2400679.

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When type II pneumonocytes were exposed to purified lung surfactant that contained 1-palmitoyl-2-[3H]palmitoyl-glycero-3-phosphocholine, radiolabelled surfactant was apparently taken up by the cells since it could not be removed by either repeated washing or exchange with non-radiolabelled surfactant, but was released when the cells were lysed. After 4 h of exposure to [3H]surfactant, more than half of the 3H within cells remained in disaturated phosphatidylcholine. Incorporation of [3H]choline, [14C]palmitate and [14C]acetate into glycerophospholipids was decreased in type II cells exposed to

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22

Rüdiger, Mario, Angelika Tölle, Wolfgang Meier, and Bernd Rüstow. "Naturally derived commercial surfactants differ in composition of surfactant lipids and in surface viscosity." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 2 (2005): L379—L383. http://dx.doi.org/10.1152/ajplung.00176.2004.

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Pulmonary surfactant biophysical properties are best described by surface tension and surface viscosity. Besides lecithin, surfactant contains a variety of minor lipids, such as plasmalogens, polyunsaturated fatty acid-containing phospholipids (PUFA-PL), and cholesterol. Plasmalogens and cholesterol improve surface properties of lipid mixtures significantly. High PUFA-PL and plasmalogen content in tracheal aspirate of preterm infants reduces the risk of developing chronic lung disease. Different preparations are available for exogenous surfactant substitution; however, little is known about li

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23

Haddad, I. Y., H. Ischiropoulos, B. A. Holm, J. S. Beckman, J. R. Baker, and S. Matalon. "Mechanisms of peroxynitrite-induced injury to pulmonary surfactants." American Journal of Physiology-Lung Cellular and Molecular Physiology 265, no. 6 (1993): L555—L564. http://dx.doi.org/10.1152/ajplung.1993.265.6.l555.

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Activated alveolar macrophages secrete both nitric oxide and superoxide in the alveolar lining fluid which combine rapidly to form peroxynitrite, a potent oxidizing agent capable of damaging lipids and proteins in biological membranes. Peroxynitrite (1 mM) plus 100 microM Fe3+EDTA inhibited calf lung surfactant extract (CLSE) from reaching a minimum surface tension below 10 mN/m on dynamic compression. Peroxynitrite and its by-products reacted with the unsaturated lipid components of CLSE, as evidenced by the appearance of conjugated dienes and thiobarbituric acid products, and damaged all sur

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24

Van Golde, L. M. G. "Synthesis of Surfactant Lipids in the Adult Lung." Annual Review of Physiology 47, no. 1 (1985): 765–74. http://dx.doi.org/10.1146/annurev.ph.47.030185.004001.

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25

Fisher, A. B., and A. Chander. "Intracellular Processing of Surfactant Lipids in the Lung." Annual Review of Physiology 47, no. 1 (1985): 789–802. http://dx.doi.org/10.1146/annurev.ph.47.030185.004041.

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26

Quintero, Omar A., and Jo Rae Wright. "Metabolism of phosphatidylglycerol by alveolar macrophages in vitro." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 2 (2000): L399—L407. http://dx.doi.org/10.1152/ajplung.2000.279.2.l399.

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In whole animal studies, it has been shown that turnover of surfactant dipalmitoylphosphatidylglycerol (DPPG) is faster than that of dipalmitoylphosphatidylcholine (DPPC). The goal of this investigation was to characterize the metabolism of DPPG by alveolar macrophages and to determine whether they contribute to the faster alveolar clearance of DPPG. Isolated rat alveolar macrophages were incubated with liposomes colabeled with [3H]DPPG and [14C]DPPC. Macrophages internalized both lipids in a time- and temperature-dependent manner. The uptake of both lipids was increased by surfactant protein

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27

Haddad, I. Y., S. Zhu, H. Ischiropoulos, and S. Matalon. "Nitration of surfactant protein A results in decreased ability to aggregate lipids." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 2 (1996): L281—L288. http://dx.doi.org/10.1152/ajplung.1996.270.2.l281.

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We assessed the extent to which nitration of surfactant protein (SP) A, isolated from the bronchoalveolar lavage of patients with alveolar proteinosis, alters its ability to enhance lipid aggregation, bind lipids, and act synergistically with surfactant apoproteins B and C (SP-B, SP-C) in lowering the surface activity of surfactant lipids. SP-A was treated with various concentrations of tetranitromethane (TNM) at pH 6, 7.4, 8, or 10. Depending on the pH, TNM acts either as a nitrating (pH > or = 7.4) or an oxidizing agent (pH < or = 6). Exposure of SP-A to TNM (0.1-1 mM) at pH 7.4 or 8 f

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28

Kremlev, S. G., T. M. Umstead, and D. S. Phelps. "Effects of surfactant protein A and surfactant lipids on lymphocyte proliferation in vitro." American Journal of Physiology-Lung Cellular and Molecular Physiology 267, no. 4 (1994): L357—L364. http://dx.doi.org/10.1152/ajplung.1994.267.4.l357.

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We studied the effects of dipalmitoyl L-alpha-phosphatidylcholine (DPPC), Survanta, surfactant protein A (SP-A), and mixtures of these substances on mitogen-induced lymphocyte proliferation using concanavalin A as a mitogen. A concentration-dependent suppression of proliferation was observed with 50-250 micrograms/ml of DPPC or Survanta. However, when SP-A was added to cultures, proliferation was stimulated. The inhibitory effects of DPPC and Survanta were altered in mixtures that contained SP-A. When added to 50 micrograms/ml of Survanta, SP-A reversed the inhibitory influence of Survanta and

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29

Liau, Deng F., and Stephen F. Ryan. "Purification of surfactant protein A from dog lung by reconstitution with surfactant lipids." Chemistry and Physics of Lipids 59, no. 1 (1991): 29–38. http://dx.doi.org/10.1016/0009-3084(91)90060-o.

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30

Palaniyar, Nades, Ross A. Ridsdale, Stephen A. Hearn, Fred Possmayer, and George Harauz. "Formation of membrane lattice structures and their specific interactions with surfactant protein A." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 4 (1999): L642—L649. http://dx.doi.org/10.1152/ajplung.1999.276.4.l642.

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Biological membranes exist in many forms, one of which is known as tubular myelin (TM). This pulmonary surfactant membranous structure contains elongated tubes that form square lattices. To understand the interaction of surfactant protein (SP) A and various lipids commonly found in TM, we undertook a series of transmission-electron-microscopic studies using purified SP-A and lipid vesicles made in vitro and also native surfactant from bovine lung. Specimens from in vitro experiments were negatively stained with 2% uranyl acetate, whereas fixed native surfactant was delipidated, embedded, and s

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31

Wright, J. R. "Immunomodulatory functions of surfactant." Physiological Reviews 77, no. 4 (1997): 931–62. http://dx.doi.org/10.1152/physrev.1997.77.4.931.

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The possibility that the lipoprotein complex of lung surfactant functions in pulmonary host defense as well as lowering surface tension at the air-liquid interface has been the subject of renewed interest in light of the finding that surfactant proteins A and D (SP-A and SP-D) are members of a family of proteins known as collectins. The collectins, so named because they have in common an NH2-terminal collagen-like domain and a COOH-terminal lectin (carbohydrate binding) domain, are found in both lung and serum and participate in "innate" immunity, acting before induction of an antibody-mediate

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32

Veldhuizen, R. A., S. A. Hearn, J. F. Lewis, and F. Possmayer. "Surface-area cycling of different surfactant preparations: SP-A and SP-B are essential for large-aggregate integrity." Biochemical Journal 300, no. 2 (1994): 519–24. http://dx.doi.org/10.1042/bj3000519.

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Surface-area cycling is an in vitro procedure for the conversion of large into small surfactant aggregates. In this procedure a tube containing a surfactant suspension is rotated end-over-end at 37 degrees C so that the surface area of the suspension changes twice each cycle. We have utilized this method to study the mechanisms involved in aggregate conversion. Several different surfactant preparations were analysed: (1) bovine natural surfactant, a sucrose-gradient-purified material containing surfactant phospholipid and surfactant-associated proteins (SP-) SP-A, SP-B and SP-C; (2) bovine lip

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33

Walker, S. R., M. C. Williams, and B. Benson. "Immunocytochemical localization of the major surfactant apoproteins in type II cells, Clara cells, and alveolar macrophages of rat lung." Journal of Histochemistry & Cytochemistry 34, no. 9 (1986): 1137–48. http://dx.doi.org/10.1177/34.9.2426341.

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The adsorptive properties of phospholipids of pulmonary surfactant are markedly influenced by the presence of three related proteins (26-38 KD, reduced) found in purified surfactant. Whether these proteins are pre-assembled with lipids before secretion is uncertain but would be expected for a lipoprotein secretion. We performed indirect immunocytochemistry on frozen thin sections of rat lung to identify cells and intracellular organelles that contain these proteins. The three proteins, purified from lavaged surfactant, were used to generate antisera in rabbits. Immunoblotting of rat surfactant

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34

Walther, Frans J., Monik Gupta, Michael M. Lipp, et al. "Aerosol delivery of dry powder synthetic lung surfactant to surfactant-deficient rabbits and preterm lambs on non-invasive respiratory support." Gates Open Research 3 (January 14, 2019): 6. http://dx.doi.org/10.12688/gatesopenres.12899.1.

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Background: The development of synthetic lung surfactant for preterm infants has focused on peptide analogues of native surfactant proteins B and C (SP-B and SP-C). Non-invasive respiratory support with nasal continuous positive airway pressure (nCPAP) may benefit from synthetic surfactant for aerosol delivery. Methods: A total of three dry powder (DP) surfactants, consisting of phospholipids and the SP-B analogue Super Mini-B (SMB), and one negative control DP surfactant without SMB, were produced with the Acorda Therapeutics ARCUS® Pulmonary Dry Powder Technology. Structure of the DP surfact

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35

Walther, Frans J., Monik Gupta, Michael M. Lipp, et al. "Aerosol delivery of dry powder synthetic lung surfactant to surfactant-deficient rabbits and preterm lambs on non-invasive respiratory support." Gates Open Research 3 (March 14, 2019): 6. http://dx.doi.org/10.12688/gatesopenres.12899.2.

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Background: The development of synthetic lung surfactant for preterm infants has focused on peptide analogues of native surfactant proteins B and C (SP-B and SP-C). Non-invasive respiratory support with nasal continuous positive airway pressure (nCPAP) may benefit from synthetic surfactant for aerosol delivery. Methods: A total of three dry powder (DP) surfactants, consisting of phospholipids and the SP-B analogue Super Mini-B (SMB), and one negative control DP surfactant without SMB, were produced with the Acorda Therapeutics ARCUS® Pulmonary Dry Powder Technology. Structure of the DP surfact

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36

Minoo, P., R. J. King, and J. J. Coalson. "Surfactant proteins and lipids are regulated independently during hyperoxia." American Journal of Physiology-Lung Cellular and Molecular Physiology 263, no. 2 (1992): L291—L298. http://dx.doi.org/10.1152/ajplung.1992.263.2.l291.

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Adult hamsters were exposed to 100% oxygen for up to 8 days. At time of death lung tissue was analyzed for the expression of surfactant protein (SP) genes, and surfactant was isolated from alveolar lavage fluid. Surfactant was analyzed for the composition of proteins and phospholipids and for its surface properties. We found, over the 8 days of exposure, that an alveolitis composed of polymorphonuclear leukocytes (PMNs) and alveolar macrophages, accompanied by exudation of edema fluid, appeared in the alveolar spaces. The steady-state levels of SP mRNAs declined after 8 days of exposure to 100

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37

Dietl, Paul, and Manfred Frick. "Channels and Transporters of the Pulmonary Lamellar Body in Health and Disease." Cells 11, no. 1 (2021): 45. http://dx.doi.org/10.3390/cells11010045.

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The lamellar body (LB) of the alveolar type II (ATII) cell is a lysosome-related organelle (LRO) that contains surfactant, a complex mix of mainly lipids and specific surfactant proteins. The major function of surfactant in the lung is the reduction of surface tension and stabilization of alveoli during respiration. Its lack or deficiency may cause various forms of respiratory distress syndrome (RDS). Surfactant is also part of the innate immune system in the lung, defending the organism against air-borne pathogens. The limiting (organelle) membrane that encloses the LB contains various transp

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38

López, O., M. Cócera, R. Pons, et al. "Use of Synchrotron Radiation SAXS to Study the First Steps of the Interaction between Sodium Dodecyl Sulfate and Charged Liposomes." Spectroscopy 16, no. 3-4 (2002): 343–50. http://dx.doi.org/10.1155/2002/714548.

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The technique of time resolved small angle X–ray scattering (SAXS) using a synchrotron radiation source was used to study the structural transformations as well as the kinetic associated with the first steps of the solubilization of liposomes induced by the anionic surfactant sodium dodecyl sulfate (SDS). Neutral and electrically charged (anionic and cationic) liposomes were used to investigate the effect of the electrostatic charges on these initial steps. The mechanism that induces the solubilization process consisted in an adsorption of surfactant on the bilayers and a desorption of mixed m

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Kremlev, S. G., and D. S. Phelps. "Surfactant protein A stimulation of inflammatory cytokine and immunoglobulin production." American Journal of Physiology-Lung Cellular and Molecular Physiology 267, no. 6 (1994): L712—L719. http://dx.doi.org/10.1152/ajplung.1994.267.6.l712.

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Pulmonary surfactant plays a variety of roles related to the regulation of immune function in the lung. Of particular interest in this regard is surfactant protein A (SP-A), a calcium-dependent lectin. We have reported previously that SP-A enhances concanavalin A-induced proliferation, and in this study we examined the secretion of tumor necrosis factor-alpha (TNF-alpha), interleukins 1 alpha, 1 beta, and 6, and interferon-gamma by human peripheral blood mononuclear cells. Levels of all of the cytokines except interferon-gamma were increased by SP-A. In rat peripheral blood cells, splenocytes,

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Quintero, Omar A., and Jo Rae Wright. "Clearance of surfactant lipids by neutrophils and macrophages isolated from the acutely inflamed lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 282, no. 2 (2002): L330—L339. http://dx.doi.org/10.1152/ajplung.00190.2001.

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Pulmonary surfactant reduces surface tension at the lung air-liquid interface and defends the host against infection. Several lines of evidence show that surfactant levels are altered in animal models and patients with inflammatory or infectious lung diseases. We tested the hypothesis that cells responding to lung injury alter surfactant levels through increased phospholipid clearance. Acute lung injury was induced by intratracheal administration of lipopolysaccharide (LPS; Escherichia coli026:B6) into rats. LPS exposure resulted in a 12-fold increase in the number of cells isolated by lavage,

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Pérez-Gil, Jesus, Jacqueline Tucker, Gary Simatos, and Kevin M. W. Keough. "Interfacial adsorption of simple lipid mixtures combined with hydrophobic surfactant protein from pig lung." Biochemistry and Cell Biology 70, no. 5 (1992): 332–38. http://dx.doi.org/10.1139/o92-051.

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Hydrophobic pulmonary surfactant protein enriched in SP-C has been mixed in amounts up to 10% by weight with various phospholipids. The lipids used were dipalmitoyl phosphatidylcholine (DPPC), or DPPC plus unsaturated phosphatidylglycerol (PG), or phosphatidylinositol (PI) in molar ratios of 9:1 and 7:3. The protein enhanced the rate and extent of adsorption of each lipid preparation into the air–water interface, and its respreading after compression on a surface balance. Maximum surface pressures attained on compression of monolayers of mixtures of lipids were slightly higher in the presence

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Rustow, B., R. Haupt, P. A. Stevens, and D. Kunze. "Type II pneumocytes secrete vitamin E together with surfactant lipids." American Journal of Physiology-Lung Cellular and Molecular Physiology 265, no. 2 (1993): L133—L139. http://dx.doi.org/10.1152/ajplung.1993.265.2.l133.

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Lung surfactant is exposed to strongly oxidizing conditions. We examined the hypothesis that in lung, lipophilic antioxidants are secreted together with surfactant to counteract the peroxidation of surfactant constituents. Lung lavage and the subfractions of the alveolar surfactant contain the lipophilic antioxidants vitamin E, vitamin A, and plasmalogens. The specific radioactivity of vitamin E isolated from serum, lung homogenate, lamellar bodies, and lung lavage increased linearly up to 3 h after intraperitoneal application of [3H]tocopherol. [3H]tocopherol was secreted in situ together wit

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Stachowicz-Kuśnierz, A., L. Cwiklik, J. Korchowiec, E. Rogalska, and B. Korchowiec. "The impact of lipid oxidation on the functioning of a lung surfactant model." Physical Chemistry Chemical Physics 20, no. 38 (2018): 24968–78. http://dx.doi.org/10.1039/c8cp04496a.

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Rochman, M. Fatchur, Aditya Darmawan, and Pramudya Wardhana. "Nanostructured Lipid Carriers System Solid Lipid Poloxamer and Stearic Acid with Liquid Lipid Soybean Oil." Jurnal Ilmiah Medicamento 8, no. 1 (2022): 1–7. http://dx.doi.org/10.36733/medicamento.v8i1.3161.

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Nanostructured Lipid Carriers (NLC) are lipid-based carrier system that use a matrix combination in the form of solid and liquid which are stabilized with the addition of surfactant. This NLC was developed to facilitate the dispersion of hydrophobic bioactive compound in a hydrophilic system. This research aims to get the right formulation and can develop stable characterization, using solid lipids Poloxamer and Stearic Acid with liquid lipids Soybeans Oil using surfactant Tween 80 and co-surfactant Propyleneglycol.. The to make the formulation of NLC with a ratio of poloxamer and stearic acid

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Shamsieva, Elena V., Svetlana A. Lukina, and Marina R. Timofeeva. "The effect of the imbalance of the neurotransmitter systems of the dorsal hippocampus on the activity of alveolar macrophages and lung surfactant." Journal of Ural Medical Academic Science 19, no. 4 (2022): 412–20. http://dx.doi.org/10.22138/2500-0918-2022-19-4-412-420.

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The purpose of the study. The paper analyzes the metabolism of surfactant lipids and phagocytic activity of alveolar macrophages with an imbalance of the neurotransmitter systems of the dorsal hippocampus. Materials and methods. Male rats were microinjected with L-glutamate and GABA into the dorsal hippocampus bilaterally by stereotactic coordinates. Studies included determination of surfactant lipid fractions (thin-layer chromatography method), total phospholipids and their surface-active properties (Wilhelmi method), phospholipase activity, evaluation of endopulmonary cytogram, phagocytic in

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Hidayat, Nur, and Luqman Nur Chandra. "Selection of Pseudomonas sp. for Lipid and Detergent Degradation." Agroindustrial Journal 3, no. 1 (2017): 121. http://dx.doi.org/10.22146/aij.v3i1.25027.

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The objective of the research was to identify which Pseudomonas species has the ability to alter lipids and surfactants simultaneously. This research was conducted by using three Pseudomonas species, vegetable oil, and commercial detergent which contains Linear Alkyl Sulfonate LAS. The result shows that Pseudomonas aeruginosa is able to reduce lipids and surfactant 80.53% and 61.22% respectively.

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Rider, Evelyn D., Machiko Ikegami, Kent E. Pinkerton, Janice L. Peake, and Alan H. Jobe. "Lysosomes from rabbit type II cells catabolize surfactant lipids." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 1 (2000): L68—L74. http://dx.doi.org/10.1152/ajplung.2000.278.1.l68.

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The role of a lysosome fraction from rabbit type II cells in surfactant dipalmitoylphosphatidylcholine (DPPC) catabolism was investigated in vivo using radiolabeled DPPC and dihexadecylphosphatidylcholine (1,2-dihexadecyl- sn-glycero-3-phosphocholine; DEPC), a phospholipase A1- and A2-resistant analog of DPPC. Freshly isolated type II cells were gently disrupted by shearing, and lysosomes were isolated with Percoll density gradients (density range 1.0591–1.1457 g/ml). The lysosome fractions were relatively free of contaminating organelles as determined by electron microscopy and organelle mark

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LODEN, M., and A. C. ANDERSSON. "Effect of topically applied lipids on surfactant-irritated skin." British Journal of Dermatology 134, no. 2 (1996): 215–20. http://dx.doi.org/10.1046/j.1365-2133.1996.978714.x.

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LODEN, M., and A. C. ANDERSSON. "Effect of topically applied lipids on surfactant-irritated skin." British Journal of Dermatology 134, no. 2 (1996): 215–20. http://dx.doi.org/10.1111/j.1365-2133.1996.tb07604.x.

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Tyman, John H. P., and Ian E. Bruce. "Surfactant properties and biodegradation of polyethoxylates from phenolic lipids." Journal of Surfactants and Detergents 7, no. 2 (2004): 169–73. http://dx.doi.org/10.1007/s11743-004-0300-3.

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