Stabilization of lung surfactant particles against conversion by a cycling interface

1997 ◽  
Vol 272 (2) ◽  
pp. L335-L343 ◽  
Author(s):  
S. B. Hall ◽  
R. W. Hyde ◽  
M. C. Kahn
Keyword(s):  
Pulmonary Surfactant ◽  
Distress Syndrome ◽  
Proteinase Inhibitors ◽  
Lung Surfactant ◽  
Small Particles ◽  
Active Particles ◽  
Large Particles ◽  
Differential Sedimentation ◽  
Proteinase Inhibition

The large active particles of pulmonary surfactant are depleted in patients with acute respiratory distress syndrome and in animal models of this disorder. We studied in vitro conversion of large to small particles, separated by differential sedimentation, to determine how factors lavaged from rabbits injured by intravenous oleic acid would affect conversion. In half-filled test tubes rotated end over end, samples from injured animals increased the recovery of large particles from 40 +/- 6% of uncycled samples for controls to 62 +/- 21%. We hypothesized that proteins in the injured samples, and perhaps also the proteinase inhibitors used previously to block conversion (N. J. Gross and R. M. Schultz. Biochim. Biophys. Acta 1044: 222-230, 1990), stabilized surfactant particles by limiting access to the cycling interface. Hemoglobin, neutrophil elastase, and alpha1-antiproteinase (alpha1-PI) oxidized to eliminate its antiproteinase activity all stabilized large particles against conversion. Hemoglobin was most effective, increasing recovery from 18 +/- 5% for controls to 86 +/- 5% with 0.4 mg/ml hemoglobin. Native alpha1-PI had no effect on conversion. Our results suggest that acceleration of normal conversion is unlikely to explain the depletion of large particles in injured lungs. They also suggest that conversion of surfactant particles separated by differential sedimentation requires no proteinase susceptible to inhibition by alpha1-PI. They provide an alternate hypothesis related to interfacial effects rather than proteinase inhibition for the previously reported effect of alpha1-PI on conversion of particles separated according to density.

scholarly journals In vitro activity of the clinical pulmonary surfactant Surfacen® against Leishmania amazonensis

2011 ◽  
Vol 53 (4) ◽  
pp. 235-238 ◽  
Author(s):  
Odalys Blanco ◽  
Yuliannis Lugones ◽  
Elaine Díaz ◽  
Lianet Monzote
Keyword(s):  
Respiratory Distress Syndrome ◽  
Pulmonary Surfactant ◽  
Distress Syndrome ◽  
Lung Surfactant ◽  
Peritoneal Macrophages ◽  
Leishmania Amazonensis ◽  
Vitro Activity ◽  
In Vitro Activity ◽  
Ic50 Value

Surfacen® is an exogenous natural lung surfactant, composed by phospholipids and hydrophobic proteins, which is applied successfully in Newborn Respiratory Distress Syndrome. In this paper, in vitro activity of Surfacen® against Leishmania amazonensis is described. The product showed activity against the amastigote form found in peritoneal macrophages from BALB/c mice, with an IC50 value of 17.9 ± 3.0 µg/mL; while no toxic effect on host cell was observed up to 200 µg/mL. This is the first report about the antileishmanial activity of Surfacen®.

Alterations in the surface properties of lung surfactant in the torpid marsupial Sminthopsis crassicaudata

1998 ◽  
Vol 84 (1) ◽  
pp. 146-156 ◽  
Author(s):  
Olga V. Lopatko ◽  
Sandra Orgeig ◽  
Christopher B. Daniels ◽  
David Palmer
Keyword(s):  
Surface Tension ◽  
Surface Properties ◽  
Surface Activity ◽  
Pulmonary Surfactant ◽  
Lung Surfactant ◽  
Lung Compliance ◽  
Equilibrium Surface Tension ◽  
Sminthopsis Crassicaudata

Lopatko, Olga V., Sandra Orgeig, Christopher B. Daniels, and David Palmer. Alterations in the surface properties of lung surfactant in the torpid marsupial Sminthopsis crassicaudata. J. Appl. Physiol. 84(1): 146–156, 1998.—Torpor changes the composition of pulmonary surfactant (PS) in the dunnart Sminthopsis crassicaudata [C. Langman, S. Orgeig, and C. B. Daniels. Am. J. Physiol. 271 ( Regulatory Integrative Comp. Physiol. 40): R437–R445, 1996]. Here we investigated the surface activity of PS in vitro. Five micrograms of phospholipid per centimeter squared surface area of whole lavage (from mice or from warm-active, 4-, or 8-h torpid dunnarts) were applied dropwise onto the subphase of a Wilhelmy-Langmuir balance at 20°C and stabilized for 20 min. After 4 h of torpor, the adsorption rate increased, and equilibrium surface tension (STeq), minimal surface tension (STmin), and the %area compression required to achieve STmin decreased, compared with the warm-active group. After 8 h of torpor, STmin decreased [from 5.2 ± 0.3 to 4.1 ± 0.3 (SE) mN/m]; %area compression required to achieve STmindecreased (from 43.4 ± 1.0 to 27.4 ± 0.8); the rate of adsorption decreased; and STeqincreased (from 26.3 ± 0.5 to 38.6 ± 1.3 mN/m). ST-area isotherms of warm-active dunnarts and mice at 20°C had a shoulder on compression and a plateau on expansion. These disappeared on the isotherms of torpid dunnarts. Samples of whole lavage (from warm-active and 8-h torpor groups) containing 100 μg phospholipid/ml were studied by using a captive-bubble surfactometer at 37°C. After 8 h of torpor, STmin increased (from 6.4 ± 0.3 to 9.1 ± 0.3 mN/m) and %area compression decreased in the 2nd (from 88.6 ± 1.7 to 82.1 ± 2.0) and 3rd (from 89.1 ± 0.8 to 84.9 ± 1.8) compression-expansion cycles, compared with warm-active dunnarts. ST-area isotherms of warm-active dunnarts at 37°C did not have a shoulder on compression. This shoulder appeared on the isotherms of torpid dunnarts. In conclusion, there is a strong correlation between in vitro changes in surface activity and in vivo changes in lipid composition of PS during torpor, although static lung compliance remained unchanged (see Langman et al. cited above). Surfactant from torpid animals is more active at 20°C and less active at 37°C than that of warm-active animals, which may represent a respiratory adaptation to low body temperatures of torpid dunnarts.

Role of the Lung Surfactant in the Treatment of Sars-Cov-2 Infection

2020 ◽  
pp. 1-6
Author(s):  
Bruno Riccardi ◽  
◽  
Thomas De Paoli ◽  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Pulmonary Surfactant ◽  
Distress Syndrome ◽  
Lung Surfactant ◽  
Hyaline Membrane Disease ◽  
Hyaline Membrane ◽  
Current Therapies ◽  
Preterm Babies ◽  
First Time

The spread of SARS-CoV2 has been progressing continuously for over eight months. Numerous treatments have been proposed, and many have shown efficacy and ability to control the Covid-19 syndrome in this study we propose for the first time, the use of replacement therapy with Pulmonary Surfactant (PS), in patients admitted to intensive care. Pulmonary Surfactant is widely used to treat Acute Respiratory Distress Syndrome (ARDS) in preterm babies and has shown remarkable therapeutic efficacy. Since ARDS, also known as hyaline membrane disease, has many pathogenetic and symptomatological similarities with those produced by SARS-CoV2 infection, it may be useful to associate adjuvant therapy with Pulmonary Surfactant to current therapies in use. The Surfactant that we propose in our study can act as a carrier to convey even drugs with reduced absorption and poor bioavailability, directly in the most hidden alveolar areas.

Surfactant-associated protein inhibits phospholipid secretion from type II cells

1987 ◽  
Vol 63 (2) ◽  
pp. 692-698 ◽  
Author(s):  
W. R. Rice ◽  
G. F. Ross ◽  
F. M. Singleton ◽  
S. Dingle ◽  
J. A. Whitsett
Keyword(s):  
Pulmonary Surfactant ◽  
Lung Surfactant ◽  
Inhibitory Effect ◽  
Heat Denaturation ◽  
Type Ii Cells ◽  
Dependent Manner ◽  
Type Ii ◽  
Inhibitory Effects ◽  
Dose Dependent

Secretion of [3H]phosphatidylcholine ([3H]PC) from isolated rat pulmonary type II epithelial cells was inhibited by the surfactant-associated protein of Mr = 35,000 (SAP-35) purified from canine lung surfactant. SAP-35 inhibited [3H]PC secretion in a dose-dependent manner and significantly inhibited basal, phorbol ester, beta-adrenergic, and P2-purinergic agonist-induced [3H]PC secretion. SAP-35 significantly inhibited [3H]PC secretion from 1 to 3 h after treatment. The IC50 for inhibition of [3H]PC secretion by canine SAP-35 was 1–5 X 10(-6) g/ml and was similar for inhibition of both basal and secretagogue-stimulated release. Heat denaturation of SAP-35, addition of monoclonal anti-SAP-35 antibody, reduction and alkylation of SAP-35, or association of SAP-35 with phospholipid vesicles reversed the inhibitory effect on secretagogue-induced secretion. Inhibitory effects of SAP-35 were observed 3 h after cells were washed with buffer that did not contain SAP-35. Although SAP-35 enhanced reassociation of surfactant phospholipid with isolated type II cells, its inhibitory effect on secretion of [3H]PC did not result from stimulation of reuptake of secreted [3H]PC by type II cells. The inhibition of phospholipid secretion by SAP-35 was also not due to inhibition of PC or disaturated PC synthesis by SAP-35. SAP-35, the major phospholipid-associated protein in pulmonary surfactant, is a potent inhibitor of surfactant secretion from type II cells in vitro and may play an important role in homeostasis of surfactant in the alveolar space.

scholarly journals Pulmonary surfactant augments cytotoxicity of silica nanoparticles: Studies on an in vitro air–blood barrier model

2015 ◽  
Vol 6 ◽  
pp. 517-528 ◽  
Author(s):  
Jennifer Y Kasper ◽  
Lisa Feiden ◽  
Maria I Hermanns ◽  
Christoph Bantz ◽  
Michael Maskos ◽  
...  
Keyword(s):  
Toxic Effect ◽  
Silica Nanoparticles ◽  
Cell Line ◽  
Surface Properties ◽  
Pulmonary Surfactant ◽  
Lung Surfactant ◽  
Membrane Integrity ◽  
Chemical Surface ◽  
The Impact

The air–blood barrier is a very thin membrane of about 2.2 µm thickness and therefore represents an ideal portal of entry for nanoparticles to be used therapeutically in a regenerative medicine strategy. Until now, numerous studies using cellular airway models have been conducted in vitro in order to investigate the potential hazard of NPs. However, in most in vitro studies a crucial alveolar component has been neglected. Before aspirated NPs encounter the cellular air–blood barrier, they impinge on the alveolar surfactant layer (10–20 nm in thickness) that lines the entire alveolar surface. Thus, a prior interaction of NPs with pulmonary surfactant components will occur. In the present study we explored the impact of pulmonary surfactant on the cytotoxic potential of amorphous silica nanoparticles (aSNPs) using in vitro mono- and complex coculture models of the air–blood barrier. Furthermore, different surface functionalisations (plain-unmodified, amino, carboxylate) of the aSNPs were compared in order to study the impact of chemical surface properties on aSNP cytotoxicity in combination with lung surfactant. The alveolar epithelial cell line A549 was used in mono- and in coculture with the microvascular cell line ISO-HAS-1 in the form of different cytotoxicity assays (viability, membrane integrity, inflammatory responses such as IL-8 release). At a distinct concentration (100 µg/mL) aSNP–plain displayed the highest cytotoxicity and IL-8 release in monocultures of A549. aSNP–NH2 caused a slight toxic effect, whereas aSNP–COOH did not exhibit any cytotoxicity. In combination with lung surfactant, aSNP–plain revealed an increased cytotoxicity in monocultures of A549, aSNP–NH2 caused a slightly augmented toxic effect, whereas aSNP–COOH did not show any toxic alterations. A549 in coculture did not show any decreased toxicity (membrane integrity) for aSNP–plain in combination with lung surfactant. However, a significant augmented IL-8 release was observed, but no alterations in combination with lung surfactant. The augmented aSNP toxicity with surfactant in monocultures appears to depend on the chemical surface properties of the aSNPs. Reactive silanol groups seem to play a crucial role for an augmented toxicity of aSNPs. The A549 cells in the coculture seem to be more robust towards aSNPs, which might be a result of a higher differentiation and polarization state due the longer culture period.

scholarly journals Potency of Meropenem-Vaborbactam in Lung Surfactant

2017 ◽  
Vol 62 (1) ◽  
Author(s):  
Debora Rubio-Aparicio ◽  
Jeff Loutit ◽  
Michael Dudley ◽  
Olga Lomovskaya
Keyword(s):  
Antibacterial Activity ◽  
Klebsiella Pneumoniae ◽  
Pulmonary Surfactant ◽  
Lung Surfactant ◽  
Gram Negative Bacteria ◽  
Gram Negative ◽  
Content Type ◽  
Fixed Concentration

ABSTRACT This study investigated whether pulmonary surfactant has an effect on the in vitro antibacterial activity of either meropenem alone or meropenem in combination with vaborbactam at a fixed concentration of 8 μg/ml against several Klebsiella pneumoniae carbapenemase (KPC)-producing strains of Gram-negative bacteria. Results showed that the potency of meropenem alone and that of meropenem-vaborbactam were not affected when tested with pulmonary surfactant.

Abnormal Structure of von Willebrand Factor in Myeloproliferative Syndrome Is Associated to Either Thrombotic or Bleeding Diathesis

1987 ◽  
Vol 58 (02) ◽  
pp. 753-757 ◽  
Author(s):  
M F López-Fernández ◽  
C López-Berges ◽  
R Martín ◽  
A Pardo ◽  
F J Ramos ◽  
...  
Keyword(s):  
Von Willebrand Factor ◽  
Proteinase Inhibitors ◽  
Relative Proportion ◽  
Variable Degree ◽  
Bleeding Diathesis ◽  
Myeloproliferative Syndrome ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryThe multimeric and subunit patterns of plasma von Willebrand factor (vWF) were analyzed in eight patients with myeloproliferative syndrome (MS) in order to investigate the possible existence of heterogeneity in the “in vivo” proteolytic cleavage of the protein, previously observed in this entity. Six patients lacked large vWF multimers, five of them having normal bleeding times (BT) and clinically documented episodes of thrombotic origin, whereas one patient had long BT and bleeding symptoms. Seven patients showed a relative increase in the 176 kDa subunit fragment while the 189 kDa polypeptide was increased in only one. In addition, another patient (and prior to any therapy) showed the presence of a new fragment of approximately 95 kDa which disappeared after Busulfan therapy. The collection of blood from these patients with proteinase inhibitors did not correct the abnormalities.The infusion of DDAVP to two patients with abnormal vWF was accompanied by: the appearance of larger vWF multimers which disappeared rapidly from plasma; an increase in the relative proportion of the satellite bands of each multimer and a further increase of the 176 kDa fragment. These data point to some heterogeneity in the vWF abnormality present in MS which may be related in part to a variable degree of proteolysis of vWF occurring “in vivo” rather than “in vitro”, and which may be associated to either a thrombotic or a bleeding diathesis. They also suggest that despite the presence of abnormal, already proteolyzed vWF, DDAVP-enhanced proteolysis occurs in MS to a similar extent to what is described in normal individuals.

Chorioamnionitis alters lung surfactant lipidome in newborns with respiratory distress syndrome

2021 ◽  
Author(s):  
Sonia Giambelluca ◽  
Giovanna Verlato ◽  
Manuela Simonato ◽  
Luca Vedovelli ◽  
Luca Bonadies ◽  
...  
Keyword(s):  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Lung Surfactant
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