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At least 19 recordsLinked to original sources
PubMed2001

Dipalmitoylphosphatidylcholine and cholesterol in monolayers spread from adsorbed films of pulmonary surfactant.

Pulmonary surfactant forms a surface film that consists of a monolayer and a monolayer-associated reservoir. The extent to which surfactant components including the main component, dipalmitoylphosphatidylcholine (DPPC), are adsorbed into the monolayer, and how surfactant protein SP-A affects their adsorptions, is not clear. Transport of cholesterol to the surface region from dispersions of bovine lipid extract surfactant [BLES(chol)] with or without SP-A at 37 degrees C was studied by measuring surface radioactivities of [4-(14)C]cholesterol-labeled BLES(chol), and the Wilhelmy plate technique was used to monitor adsorption of monolayers. Results showed that transport of cholesterol was lipid concentration dependent. SP-A accelerated lipid adsorption but suppressed the final level of cholesterol in the surface. Surfactant adsorbed from a dispersion with or without SP-A was transferred via a wet filter paper to a clean surface, where the surface radioactivity and surface tension were recorded simultaneously. It was observed that 1) surface radioactivity was constant over a range of dispersion concentrations; 2) cholesterol and DPPC were transferred simultaneously; and 3) SP-A limited transfer of cholesterol. These results indicate that non-DPPC components of pulmonary surfactant can be adsorbed into the monolayer. Studies in the transfer of [1-(14)C]DPPC-labeled BLES(chol) to an equal or larger clean surface area revealed that SP-A did not increase selective adsorption of DPPC into the monolayer. Evaluation of transferred surfactant with a surface balance indicated that it equilibrated as a monolayer. Furthermore, examination of transferred surfactants from dispersions with and without prespread BLES(chol) monolayers revealed a functional contiguous association between adsorbed monolayers and reservoirs.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1993

Genetically engineered human pulmonary surfactant.

Pulmonary surfactant is a complex array of phospholipids and proteins that specifically interact to lower the surface tension in the alveoli of the lungs. This article reviews pulmonary surfactant proteins A, B, and C. Also surfactant replacement in animal studies is discussed.

Animals↗
PubMed1998

The role of lipids in pulmonary surfactant.

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.

Animals↗
PubMed2006

Electrical surface potential of pulmonary surfactant.

Pulmonary surfactant is a mixed lipid protein substance of defined composition that self-assembles at the air-lung interface into a molecular film and thus reduces the interfacial tension to close to zero. A very low surface tension is required for maintaining the alveolar structure. The pulmonary surfactant film is also the first barrier for airborne particles entering the lung upon breathing. We explored by frequency modulation Kelvin probe force microscopy (FM-KPFM) the structure and local electrical surface potential of bovine lipid extract surfactant (BLES) films. BLES is a clinically used surfactant replacement and here served as a realistic model surfactant system. The films were distinguished by a pattern of molecular monolayer areas, separated by patches of lipid bilayer stacks. The stacks were at positive electrical potential with respect to the surrounding monolayer areas. We propose a particular molecular arrangement of the lipids and proteins in the film to explain the topographic and surface potential maps. We also discuss how this locally variable surface potential may influence the retention of charged or polar airborne particles in the lung.

Animals↗
PubMed1989

Pulmonary surfactant.

Pulmonary surfactant is a chemically heterogeneous material that provides a stable, low surface tension within the lung, thereby preventing alveolar collapse at low transpulmonary pressures. Both the lipid and the protein components of surfactant are important for establishing and maintaining a low surface tension. The composition of surfactant, the biogenesis of surfactant components, and the biologic roles of surfactant components are discussed in this brief review. Surfactant functions in adult lung disease and surfactant replacement therapy are also briefly considered.

Animals↗
PubMedDate not supplied

Cytokine stimulation by Pseudomonas aeruginosa--strain variation and modulation by pulmonary surfactant.

Pulmonary surfactant and its components are part of the first-line immune defense within the lung. Here the authors show that the surfactant protein (SP) SP-D, but not SP-A, agglutinates some clinical isolates of Pseudomonas aeruginosa and Stenotrophomonas maltophilia. No agglutination of Staphylococcus aureus or Burkholderia cepacia was observed. The SP-D-induced agglutination of P. aeruginosa was not dependent on a specific lipopolysaccharide (LPS) serotype. The authors also show that SP-D, but not SP-A, increased the tumor necrosis factor (TNF alpha) release from human monocytic cells in response to a subset of P. aeruginosa and P. aeruginosa LPS. A clinical preparation of surfactant (Alveofact) blocked the TNF alpha release from monocytic cells induced by P. aeruginosa or its LPS. SP-A reversed the inhibitory effect of Alveofact in 6/8 strains of P. aeruginosa and 2/9 preparations of P. aeruginosa LPS. SP-D did not significantly alter the TNF alpha production induced by vital P. aeruginosa in the presence of Alveofact but markedly increased the TNF alpha release induced by a preparation of rough and smooth P. aeruginosa LPS. In summary, this study shows that the immunomodulatory properties of SP-A and SP-D specifically depend on the colonizing strain of P. aeruginosa. In addition, the authors show that the function of SP-A and SP-D is modulated in the presence of surfactant lipids.

Bacterial Adhesion↗
PubMed1982

Pulmonary surfactant.

Pulmonary surfactant reduces the surface tension of the alveolar air-liquid interface, thereby providing mechanical stability and preventing alveolar atelectasis. More than 50% of surfactant is dipalmitoyl phosphatidylcholine, a material that is capable of reducing the surface tension of the alveolar interface to uniquely low values. The functions of the remaining 25% unsaturated phosphatidylcholines, 5-10% phosphatidylglycerol, 5% cholesterol, and 8-10% protein are unknown. Surfactant is synthesized by alveolar epithelial type II cells and is probably secreted as a lipoprotein complex. Lamellar bodies, which distinguish type II cells, are likely to be intracellular sites of transport of processing. The catabolism of surfactant after it is secreted into the alveolar lumen is complicated and involves different turnover times for the phosphatidylcholines, phosphatidylglycerol, and the proteins. The metabolic events are under hormonal control and may involve an interplay between beta-adrenergic agonists cAMP, and prostaglandins. In disease, such as the neonatal and adult respiratory distress syndromes, derangements in the metabolic processes may produce surfactant that is abnormal with respect to its chemical and physical properties.

Adult↗
PubMed1990

Serine proteinase requirement for the extra-cellular metabolism of pulmonary surfactant.

Pulmonary surfactant as lavaged from the alveoli exists in at least three structural subtypes, lamellar body-like, tubular myelin and vesicular forms that can be separated on the basis of their buoyant densities. Previous studies have suggested that surfactant is secreted in the lamellar body form and metabolized through the other subtypes in sequence. This metabolic sequence can be reproduced in vitro by cyclic expansion and contraction ('cycling') of the surface area of nascent surfactant at 38 degrees C. Cycling of nascent secretion, which is predominantly of lamellar body-like buoyant density, rapidly converted it to the buoyant density of tubular myelin and then to that of the vesicular subtype. We examined the role of proteinases in the conversion of nascent surfactant subtypes in vitro. Addition of metallo-, cysteine- and acid-proteinase inhibitors to the cycling mix did not inhibit the conversion of tubular myelin to vesicular subtype. However, a variety of serine proteinase inhibitors inhibited the formation of vesicular subtype. Their inhibitory effect was dose-related and most marked for alpha 1-antitrypsin where a concentration equal to that found in the alveolar fluid lining layer resulted in 50% inhibition of the generation of light subtype, suggesting physiological relevance. The enzyme(s) responsible for promoting the generation of light subtype was sedimentable and therefore presumably in particulate form. By differential centrifugation of lung secretions it was separable from alveolar macrophages and partially separable from surfactant itself. It has not been identified, nor has its substrate. We conclude that in vitro cycling provides a model for the study of alveolar surfactant metabolism and that the conversion of tubular myelin to vesicular forms of surfactant requires serine proteinase activity.

Animals↗
PubMedDate not supplied

[Treatment of respiratory distress syndrome in premature infants with pulmonary surfactant].

Pulmonary surfactant contains lipids and less than 10% proteins. A number of bio-physical properties such as surface-tension lowering and spreading properties are thought to be important for function. Natural surfactants from animal lungs or human amniotic fluid have been used either for prophylaxis or therapy of RDS in very low birthweight infants. Carefully controlled clinical studies demonstrated beneficial effects in infants with RDS after natural surfactants. The main benefits were an improvement in oxygenation, a reduction in bronchopulmonary dysplasia and a reduction in mortality. The results of 5 studies using artificial surfactants clearly are in conflict with respect to short and long term benefits. As no adverse side effects after treatment with natural surfactants were observed until now, these preparations should be considered for prophylaxis or treatment of RDS.

Clinical Trials as Topic↗
PubMed1990

Low-molecular-weight hydrophobic proteins from bovine pulmonary surfactant.

Pulmonary surfactant stabilizes the lung by reducing the surface tension in the terminal air spaces. Lipid extract surfactant contains approx. 1% (w/w) low-molecular-weight hydrophobic proteins SP-B (15 kDa: nonreduced) and SP-C (3.5 kDa) and with the remainder being mainly phospholipids. The hydrophobic proteins were purified from bovine lipid extract surfactant using delipidation by phospholipase C digestion followed by hydroxyapatite chromatography. The phospholipase C step removed most of phosphatidylcholine resulting in a 10-fold enrichment of hydrophobic proteins relative to phospholipid. Chromatography of this preparation on a hydroxyapatite column resulted in the elution of phospholipids followed by SP-C and then SP-B. The column chromatography was repeated to remove residual phospholipids and yield purified SP-B and SP-C. The final recovery of SP-B from the lipid extracts was about 15-20% and that of SP-C was 5-10%. The bovine surfactant proteins were reconstituted with phospholipids and examined for their ability to lower the surface tension with a pulsating bubble surfactometer. Reconstituted surfactant preparations containing SP-B and dipalmitoylphosphatidylcholine plus dioleoylphosphatidylglycerol were capable of reducing the surface tension to near zero values at minimum bubble radius while the reconstitutes with SP-C only lowered the surface tension to approx. 20 mN/m. A more rapid decrease in surface tension was observed with reconstituted samples containing both hydrophobic proteins. These results indicate that both SP-B and SP-C can promote the adsorption and spreading of surfactant lipids at the air/liquid interface. In addition, SP-B appears to facilitate the squeeze-out of unsaturated phospholipids leading to an enrichment of dipalmitoylphosphatidylcholine in the monolayer.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1989

O2- and pneumonia-induced lung injury. II. Properties of pulmonary surfactant.

Pulmonary surfactant was isolated from the lavage fluids of animals during the course of exposure to 100% O2, 80% O2, 40% O2, or 80% O2 plus 10(8) Pseudomonas aeruginosa instilled intratracheally and analyzed for its phospholipid composition. After 4-5 days of exposure to 100% O2, disaturated phophatidylcholine (DSPC) decreased to 87% of control, whereas the ratio of phosphatidylglycerol to phosphatidylinositol (PG/PI) was 37% of control. Longer periods of ventilation with 100% O2 resulted in DSPC falling to less than 40% of control. The injury was not reversed by reducing the O2 to 50%; rather, a progressive deterioration ensued. Acute respiratory failure (ARF) induced by 5 days of bacterial infection was very similar to that seen after 5 days of exposure to 100% O2. Ventilation with 80% O2 for 6 days resulted in smaller changes in DSPC but with differences in PG/PI comparable to those seen with 100% O2 or infection. We conclude that the ability of the type II cell to synthesize surfactant of normal composition is significantly impaired in these models of ARF. The earliest index of biochemical modification is the substantial change in PG/PI, which may be predictive of early lung injury. Further exacerbation of the injury could result in the reduction of DSPC content, with subsequent changes in lung mechanics and gas exchange.

Acute Disease↗
PubMed1984

Role of calcium ions the structure and function of pulmonary surfactant.

Pulmonary surfactant isolated by centrifugation in buffers containing ions contains at least three different morphologic structures. The presence of one of these, tubular myelin, is dependent on calcium ions, since chelation of the calcium ions causes disruption of this structure. Addition of EDTA also decreases the ability of the surfactant to absorb rapidly to air-water interfaces and lower surface tension. Titration with calcium ions (2.5 or 5 mM) restores rapid surface adsorption and restores the tubular myelin structural forms. Magnesium ions cannot substitute for calcium ions in these processes. The reversibility of structure and function induced by calcium ions and EDTA is also accompanied by reversible isopycnic density shifts probably related to aggregation and disaggregation of the lipid-protein complex with calcium ions and EDTA, respectively.

Animals↗
PubMed1999

Correlated atomic force and transmission electron microscopy of nanotubular structures in pulmonary surfactant.

Pulmonary surfactant stabilizes the lung by reducing surface tension at the air-water interface of the alveoli. Surfactant is present in the lung in a number of morphological forms, including tubular myelin (TM). TM is composed of unusual 40 x 40 nm square elongated proteolipid tubes. Atomic force microscopy (AFM) was performed on polymer-embedded Lowicryl and London Resin-White (LR-White) unstained thin sections. AFM was used in imaging regions of the sections where TM was detected by transmission electron microscopy (EM) of corresponding stained sections. Tapping- and contact-mode AFM imaging of the unstained sections containing TM indicated a highly heterogeneous surface topography with height variations ranging from 10 to 100 nm. In tapping-mode AFM, tubular myelin was seen as hemispherical protrusions of 30-70 nm in diameter, with vertical dimensions of 5-8 nm. In contact-mode AFM and with phase imaging using a sharper (>10 nm nominal radius) probe, square open-ended tubes which resembled typical electron micrographs of such regions were observed. The cross-hatch structures observed inside the tubes using EM were not observed using AFM, although certain multilobe structures and topographic heterogeneity were detected inside some tubes. Other regions of multilamellar bodies and some regions where such bilayer lamella appear to fuse with the tubes were found in association with TM using AFM. EM of acetone-delipidated tubes in LR-White revealed rectangular tubular cores containing cross-hatched structures, presumably protein skeletons. AFM surface topography of these regions showed hollow depressions at positions at which the protein was anticipated instead of the protrusions seen in the lipid-containing sections. Gold-labeled antibody to surfactant protein A was found associated somewhat randomly within the regions containing the protein skeletons. The topography of the gold particles was observed as sharp peaks in contact-mode AFM. This study suggests a method for unambiguous detection of three-dimensional nanotubes present in low abundance in a biological macromolecular complex. Only limited detection of proteins and lipids in surfaces of embedded tubular myelin was possible. EM and AFM imaging of such unusual biological structures may suggest unique lipid-protein associations and arrangements in three dimensions.

Acetone↗
PubMed1982

[Drug-induced alteration of the alveolar content of pulmonary surfactant ].

Pulmonary surfactant is a lipoprotein made up mostly of tensio-active phospholipids. It is synthesized by type II pneumocytes and accumulates as lamellar bodies before being excreted into pulmonary alveoli where it fills intercellular spaces and results in a liquid film (about 1 micron thick) covering the alveolar wall. Surfactant turnover occurs through the action of phospholipases from the alveolus or pneumocytes. Level of alveolar surfactant dependents on the ratio of synthesis and degradation of its principal constituent, dipalmitoyl-phosphatidylcholine. Many substances are known to be able of alter this ratio. Among these, synthetic glucocorticosteroids appear to be the most active in increasing alveolar surfactant. The multiple possible sites of action of these steroids explain their relative efficacy in the prevention of respiratory distress in humans. Studies in progress should increase the number and the quality of drugs available for this purpose.

Adrenal Cortex Hormones↗
PubMedDate not supplied

Pulmonary surfactants in pulmonary oedema induced by head injury in mice.

A study has been carried out to examine the role of pulmonary surfactants in pulmonary oedema induced by head injury. Pulmonary oedema was induced by head injury in mice by the method of Mackay (5). There was no change in surface tension as well as total phospholipid concentration of the lung between control and test groups suggesting that there was no involvement of lung surfactant sytem in pulmonary oedema induced by head injury. Since the animals in the test group died within a few minutes, possibly there may not have been sufficient time for alteration of lung surfactant system.

Animals↗
PubMed1999

[Protective effect of exogenous pulmonary surfactant on pulmonary function during cardiopulmonary bypass in children].

OBJECTIVE: To study the protective effect of exogenous pulmonary surfactant (PS) on respiratory insufficiency after cardiopulmonary bypass in children. METHODS: 24 children of VSD associated with pulmonary hypertension undergoing heart surgery with cardiopulmonary bypass(CPB) were randomly divided into two groups: control group and PS group. In the PS group, exogenous natural porcine PS 150 mg/kg was dropped into the intracheal tube before opening the chest and removing the aortic clamp. Equal amount of normal saline was given in the control group. Lung dynamic compliance and oxygenate index were measured before and after operation. The plasma molondialdehyde(MDA) concentration of the lung was analysed perioperatively with ELISA methods. The intubation time of the two groups and ultrastructure of the lung also was measured. RESULTS: The dynamic compliance of the PS group was higher than that of the control group (P < 0.05), and the oxygenate index was significantly lower than that of the control group (P < 0.01) after CPB. Compared to the control group, the exogenous PS was able to markedly reduce the generation of MDA(P < 0.01). The intubation time of the PS group was 8.9 hours, much shorter than 13.8 hours of the control group(P < 0.001). The histological examination confirmed that the degree of pulmonary damage was significantly ameliorated in the PS group. CONCLUSION: Exogenous natural PS has protective effect on respiratory insufficiency after CPB in children with VSD associated with pulmonary hypertension.

Cardiopulmonary Bypass↗
PubMed1991

[Ultrastructural morphology of the air-blood barrier and pulmonary surfactant in pulmonary inflammation in experimental alcoholic intoxication].

Combined investigation of ultrastructure of components of air-haematic barrier and surface-active properties of surfactant in 21 guinea pigs' lungs with simulated pneumonia against a background of alcoholic intoxication was carried out. It was established, that alcoholic intoxication aggravates a deficiency of pulmonary surfactant occurred in pneumonia because of its high phagocytosis with alveolar macrophages. The increase of mobilization of alveolar macrophages in alcoholic intoxication may be connected with the rise of surfactant secretion by hyperfunctional pneumocytes of the 2nd type. Stopping of alcoholic intoxication may lead to normalization of qualitative composition of surfactant phospholipids.

Alcoholic Intoxication↗