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At least 19 recordsLinked to original sources

PubMed2000

Natural surfactant extract versus synthetic surfactant for neonatal respiratory distress syndrome.

BACKGROUND: This section is under preparation and will be included in the next issue. OBJECTIVES: To compare the effect of synthetic surfactant to natural surfactant in premature infants with established respiratory distress syndrome. SEARCH STRATEGY: Searches were made of the Oxford Database of Perinatal Trials, Medline (MeSH terms: pulmonary surfactant; limits: age groups, newborn infant; publication type, clinical trial), previous reviews including cross references, abstracts, conference and symposia proceedings, expert informants, and journal hand searching in the English language. SELECTION CRITERIA: Randomized controlled trials comparing administration of synthetic surfactants to administration of natural surfactant extracts in premature infants with respiratory distress syndrome were considered for this review. DATA COLLECTION AND ANALYSIS: Data regarding clinical outcomes including pneumothorax, patent ductus arteriosus, necrotizing enterocolitis, intraventricular hemorrhage (all intraventricular hemorrhage and severe intraventricular hemorrhage), chronic lung disease, retinopathy of prematurity, and mortality were excerpted by the primary reviewer (R. Soll). Data analysis was conducted according to the standards of the Neonatal Cochrane Review Group. MAIN RESULTS: The meta-analysis supports a significant reduction in the risk of pneumothorax (typical relative risk 0.68, 95% CI 0.56, 0.83; typical risk difference -0.04 95% CI -0.06, -0.02). No disadvantages to natural surfactant extract treatment are noted regarding other outcomes. A trend towards reduced mortality is noted in association with natural surfactant extract treatment. REVIEWER'S CONCLUSIONS: Both natural surfactant extracts and synthetic surfactant extracts are effective in the treatment of established respiratory distress syndrome. Comparative trials demonstrate greater early improvement in the requirement for ventilatory support and fewer pneumothoraces associated with natural surfactant extract treatment. On clinical grounds, natural surfactant extracts would seem to be the more desirable choice.

Biological Products↗

PubMed2006

Adsorption of mixtures of nonionic sugar-based surfactants with other surfactants at solid/liquid interfaces II. Adsorption of n-dodecyl-beta-D-maltoside with a cationic surfactant and a nonionic ethoxylated surfactant on solids.

Synergy and antagonism between sugar-based surfactants, a group of environmentally benign surfactants, and cationic surfactants and nonionic ethoxylated surfactants have been investigated in this study with solids which adsorbs only one or other when presented alone. Sugar-based n-dodecyl-beta-D-maltoside (DM) does not adsorb on silica by itself. However, in mixtures with cationic dodecyltrimethylammonium bromide (DTAB) and nonionic nonylphenol ethoxylated decyl ether (NP-10), DM adsorbs on silica through hydrophobic interactions. In contrast, although DM does adsorb on alumina, the presence of NP-10 reduces the adsorption of DM as well as that of the total surfactant adsorption. Such synergistic/antagonistic effects of sugar-based n-dodecyl-beta-D-maltoside (DM) in mixtures with other surfactants at solid/liquid interfaces were systematically investigated and some general rules on synergy/antagonism in mixed surfactant systems are identified. These results have implications for designing surfactant combinations for controlled adsorption or prevention of adsorption.

Adsorption↗

PubMed1998

Mixed Micellization of Dimeric (Gemini) Surfactants and Conventional Surfactants. I. Mixtures of an Anionic Dimeric Surfactant and of the Nonionic Surfactants C12E5 and C12E8

The mixed micellization between the anionic dimeric surfactant Dim1 (disodium 1,11-didecyl-3,6,9-trioxaundecane 1,11-disulfate) and the two nonionic surfactants C12E5 and C12E8 (penta- and octaoxyethylene monododecyl ethers, respectively) has been investigated. The cmc of the mixtures has been measured by fluorescence probing, using the fluorescent probe pyrene. Its variation with composition revealed synergism in micelle formation. The micelle aggregation (N) numbers have been measured using time-resolved fluorescence quenching at a total surfactant concentration of about 70 mM and at 25, 40, and 55°C. The differences in total aggregation number of the mixed micelles in the two systems reflect (i) the higher aggregation number of C12E5 micelles with respect to C12E8 and Dim1 micelles; (ii) the higher cloud temperature of C12E8 with respect to C12E5; and (iii) the opposite temperature dependences of N for Dim1 and nonionic surfactants micelles. The results show nonideal mixing behavior with a shallow minimum in the variation of the mixed micelle aggregation number with the mixture composition at a Dim1 mole fraction around 0.5. Copyright 1998 Academic Press. Copyright 1998Academic Press

Journal Article↗

PubMed1994

Host defence capacities of pulmonary surfactant: evidence for 'non-surfactant' functions of the surfactant system.

The most well characterized function of pulmonary surfactant is its ability to reduce surface tension at the alveolar air-liquid interface, thereby preventing lung collapse. However, several lines of evidence suggest that surfactant may also have 'non-surfactant' functions: specific components of surfactant (proteins and phospholipids) may interact with different alveolar cells, inhaled particles and micro-organisms modulating pulmonary host defence systems. SP-A, the most abundant surfactant protein, binds to alveolar macrophages via a specific surface receptor with high affinity [128]. Such binding effects the release of reactive oxygen species from resident alveolar macrophages if SP-A is properly presented to the target cell. SP-A also stimulates chemotaxis of alveolar macrophages [142], and serves as an opsonin in the phagocytosis of herpes simplex virus [161] Candida tropicalis [138] and various bacteria [137]. In addition, SP-A enhances the uptake of particles by monocytes and culture-derived macrophages [140] and improves bacterial killing. SP-D, another hydrophobic surfactant-associated protein, might interact with alveolar macrophages as well, stimulating the release of oxygen radicals [148], while for the hydrophilic surfactant proteins SP-B and SP-C no macrophage interactions have been described so far. SP-A and SP-D are members of the so-called 'collectins', pattern recognition molecules involved in first line defence. While some surfactant proteins appear to stimulate certain macrophage defence functions, surfactant phospholipids seem to inhibit those of lymphocytes. Suppressed lymphocyte functions include lymphoproliferation in response to mitogens and alloantigens, B cell immunoglobulin production and natural killer cell cytotoxicity. Concerning surfactant's phospholipid composition phosphatidylglycerol is more suppressive than phosphatidylcholine on a molar basis [38]. Bovine surfactant has an immunosuppressive effect on the development of hypersensitivity pneumonitis in a guinea pig model [150]. Despite these interesting observations, several important questions concerning the interactions of surfactant components with pulmonary host defence systems remain unanswered. Sufficient host defence in the lungs works through various humoral-cellular systems in conjunction with the specific anatomy of the airways and the gas exchange surface--how does the surfactant system fit into this network? Surfactant and alveolar cells are both altered during lung injury--is there a relationship between alveolar cells from RDS patients and the endogenous surfactant isolated from such patients? How does exogenous surfactant as used for substitution therapy modulate the defence system of the host? Some of those artificial surfactants have been shown to inhibit the endotoxin-alveolar macrophages, PMNs and monocytes including IL-1, IL-6 and TNF [139,152].(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1998

Bronchoalveolar lavage with a diluted surfactant suspension prior to surfactant instillation improves the effectiveness of surfactant therapy in experimental acute respiratory distress syndrome (ARDS).

OBJECTIVE: To assess whether bronchoalveolar lavage (BAL) with a diluted surfactant suspension prior to surfactant instillation prevents the only transient improvement in lung function as reported after surfactant instillation in severe acute respiratory distress syndrome (ARDS). DESIGN: Randomized, prospective, experimental study. SETTING: Laboratory and animal facility of a large university. MATERIALS: Adult male Sprague-Dawley rats (280 +/- 30 g). INTERVENTIONS: All animals underwent repetitive whole lung saline lavage to induce acute lung injury. Then, animals were randomly divided into seven study groups: the first group received surfactant (150 mg/ kg) within 10 min after the last lavage (early treatment), whereas in the other six groups mechanical ventilation was continued for 3 h before treatment (late treatment). Treatment consisted of: surfactant instillation at a dose of 150 mg/kg; at a dose of 250 mg/kg; BAL with saline; BAL with a diluted surfactant suspension (2.5 mg/ml); BAL with saline, immediately followed by surfactant instillation (150 mg/kg) and BAL with a diluted surfactant suspension (2.5 mg/kg), immediately followed by surfactant instillation (150 mg/kg). MEASUREMENTS AND RESULTS: Blood gases were measured for 6 h and then BAL was performed to measure the protein concentration and surface tension properties. Mean PaO2 values increased immediately after surfactant instillation to pre-lavage values but remained stable only in the group that received surfactant immediately after the lavage procedure and the group that underwent BAL with a diluted surfactant suspension prior to surfactant instillation. CONCLUSION: BAL with a diluted surfactant suspension prior to surfactant instillation at a later time point in lung injury resulted in a stable improvement of lung function. This improvement is comparable with the results seen after surfactant instillation immediately after lung lavage.

Analysis of Variance↗

PubMed1986

Hydrophobic surfactant-associated protein in whole lung surfactant and its importance for biophysical activity in lung surfactant extracts used for replacement therapy.

Hydrophobic protein of 6,000 and 14,000 daltons was isolated from mammalian pulmonary surfactant obtained from canine, human, and bovine alveolar lavage material. Low molecular weight, hydrophobic, surfactant-associated protein (SAP), herein referred to as SAP 6-14, was distinguished from SAP-35, the major glycoprotein in mammalian surfactants (the 35,000 dalton glycoprotein A or apolipoprotein A) by amino acid composition, peptide mapping, and by resistance of SAP 6-14 to digestion by endoglycosidase F, collagenase, trypsin, and other proteases. The amino acid composition of SAP 6-14 was found to be highly enriched in leucine and other hydrophobic amino acids. The characteristics of protein isolated from bovine replacement surfactant extracts utilized for the treatment of hyaline membrane disease in humans were also studied. SAP 6-14 isolated from calf lung surfactant replacement extracts (CLSE) and surfactant-TA were found to be identical to SAP 6-14 isolated from ether/ethanol extracts of various mammalian surfactants. By contrast, SAP-35, the major surfactant-associated glycoprotein of molecular weight = 35,000, and other higher molecular weight proteins were not detected in significant quantities in the CLSE or surfactant-TA replacement surfactants, either by highly sensitive silver stain analysis or by immunoblot using monospecific antisera generated against bovine SAP-35. Biophysical studies of the CLSE replacement surfactant containing only SAP 6-14 and native phospholipids demonstrated full surface activity compared to natural lung surfactant. Dynamic surface tension lowering and adsorption properties of CLSE were essentially identical to those of freshly isolated bovine whole surfactant. Thus, hydrophobic SAP 6-14 is the only protein detected in bovine lung extract surfactants with full biophysical activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Surfactant proteins and anti-surfactant antibodies in sera from infants with respiratory distress syndrome with and without surfactant treatment.

The presence of surfactant protein antigenemia and of surfactant protein antibodies was determined in serum from surfactant-treated and control infants with respiratory distress syndrome who were enrolled in a prospective randomized clinical trial. The surfactant used for treatment (surfactant TA) contained surfactant proteins (SPs) B and C and no SP-A. Enzyme-linked immunosorbent assays (ELISAs) that identify surfactant-associated proteins and ELISAs that identify IgG or IgM directed against surfactant proteins were used to investigate sera from these infants obtained prior to treatment, at 1 week of age, and at 2 months of age. There were no significant differences between average values in the surfactant-treated and control groups at each time period. However, in the control group, averaged results from ELISAs that identify SP-A and that identify IgM antibodies to SP-A or to SP-B, C showed significant differences between pretreatment sera and sera obtained at 1 week of age. No significant differences were noted in averaged results for IgG. Positive ELISA values were more frequently found in the control group than in the surfactant-treated group with regard to SP-A, and IgM against SP-A and SP-B, C in sera from neonates at 1 week of age. No positive ELISA values were found in sera from infants at 2 months of age. It is concluded that some patients with severe respiratory distress syndrome presumably leak surfactant proteins into the circulation and that this induces transient low titers of IgM antibody. This occurrence is decreased with surfactant treatment. Surfactant treatment may reduce leak of surfactant proteins into the vascular space by reducing lung damage.

Animals↗

PubMed2006

Effects of a recombinant surfactant protein-C-based surfactant on lung function and the pulmonary surfactant system in a model of meconium aspiration syndrome.

OBJECTIVE: Meconium aspiration syndrome (MAS) remains a relevant cause of neonatal respiratory failure and is characterized by severe impairment of pulmonary gas exchange, surfactant inactivation, and pronounced inflammatory changes. Surfactant administration has been shown as an effective treatment strategy in MAS. The present study aimed at investigating the impact of a recombinant surfactant protein (SP)-C-based surfactant on pulmonary gas exchange and lung function in this model of neonatal lung injury. Furthermore, SP-B and -C were determined on the transcriptional and protein level. DESIGN: Laboratory experiment. SETTING: University laboratory. SUBJECTS: Twenty three newborn piglets (median age 6 days, weight 1900-2500 g). INTERVENTIONS: Piglets were intubated and mechanically ventilated and then received 20% sterile meconium (5 mL/kg) for induction of lung injury. After 30 mins, animals were randomized for control (n = 7, MAS controls), recombinant SP-C surfactant (n = 8), or natural surfactant (n = 8). Surfactant preparations were administered as an intratracheal bolus (75 mg/kg), and animals were ventilated for another 330 mins. Nonventilated newborn piglets at term (n = 28; median weight 1484 g, range 720-1990 g) served as a healthy reference group (healthy controls). MEASUREMENTS AND MAIN RESULTS: Lung function variables, arterial blood gas samples, and lung tissues were obtained. Expression of SP-B and -C messenger RNA was quantified in left lung lobe tissue using real-time polymerase chain reaction. Protein concentrations were determined by enzyme-linked immunosorbent assay. Scanning electron microscopy and transmission electron microscopy were performed in tissue samples of the right lung lobe. Compared with healthy controls, SP-B messenger RNA expression was significantly increased in MAS (p < .02), whereas SP-C messenger RNA expression was found to be significantly reduced (p < .001). SP concentrations, however, were not significantly different. Although a significant improvement of gas exchange and lung function was observed after surfactant administration in both groups, surfactant messenger RNA expression and protein concentrations were not significantly altered. Scanning and transmission electron microscopy showed severe pulmonary ultrastructural changes after meconium aspiration improving after surfactant treatment. CONCLUSIONS: Impairment of lung function in MAS, associated with marked changes in SP messenger RNA expression, can be sufficiently treated using recombinant SP-C-based or natural surfactant. Despite improved lung function and gas exchange as well as pulmonary ultrastructure after treatment, pulmonary SP messenger RNA expression and concentrations remained significantly affected, giving important insight into the time course following surfactant treatment in MAS.

Animals↗

PubMed1999

Normal surfactant pool sizes and inhibition-resistant surfactant from mice that overexpress surfactant protein A.

Pulmonary surfactant protein-A (SP-A) has been reported to regulate the uptake and secretion of surfactant by alveolar type II cells, to stabilize large surfactant aggregates including tubular myelin, and to protect the surface activity of surfactant from protein inhibitors. In this study we investigated the consequences of overexpression of SP-A on pulmonary homeostasis and surfactant function in transgenic mice. The human SP-C promoter was used to direct synthesis of rat surfactant protein A (rSP-A) in alveolar type II cells and nonciliated bronchiolar cells of the distal respiratory epithelium. Levels of SP-A measured through enzyme-linked immunosorbent assay were 7- to 8-fold higher in lung homogenates and alveolar lavage fluid of the rSP-A mice than in those of transgene-negative littermates. The swimming exercise tolerance and lung compliance of mice bearing the transgene were unchanged. Mean air space sizes seen in randomly selected light-microscopic fields were not significantly different in the transgene-positive and -negative mice by morphometric analysis, but 15% of transgenic animals had scattered foci containing dilated alveoli and alveolar ducts without evidence of inflammation or fibrosis. Some alveolar macrophages contained bar-shaped osmophilic inclusions that had a highly ordered ultrastructure. There were no differences between the transgene-positive and -negative mice in the tissue or alveolar pool sizes of saturated phosphatidylcholine or in the large-aggregate composition of alveolar surfactant. The surface activity of surfactant isolated from the rSP-A mice was similar to that of the controls, but in the presence of protein inhibitors, the surface tension-reducing properties of the rSP-A surfactant were better preserved (P < 0.05). We conclude that overexpression of SP-A does not affect resting surfactant phospholipid levels, but that it enhances the resistance of surfactant to protein inhibition.

Animals↗

PubMed1990

Surfactant replacement therapy with a single postventilatory dose of a reconstituted bovine surfactant in preterm neonates with respiratory distress syndrome: final analysis of a multicenter, double-blind, randomized trial and comparison with similar trials. The Surfactant-TA Study Group.

The effects of a single dose of surfactant TA were assessed in premature neonates (birth weight 750 to 1749 g) with respiratory distress syndrome (RDS) in a multicenter, double-blind, randomized clinical trial. Only neonates with surfactant deficiency and without ultrasonographic evidence of intracranial hemorrhage greater than or equal to grade II were enrolled. Fifty-four patients received surfactant (100 mg of phospholipid per kilogram of body weight) and 46 patients received an air placebo within 8 hours of life. Treatment with this surfactant resulted in a significant reduction in the severity of RDS with a concomitant increase in the proportion of neonates with mild disease. The frequency of pulmonary interstitial emphysema and of pneumothorax was significantly lower in treated neonates compared with control neonates (2% vs 26%, P = .0008, and 7% vs 39%, P = .0004, respectively). The frequency of intracranial hemorrhage was significantly lower in the surfactant group compared with the control group (20% vs 54%, P = .0008) and was also reduced for the smallest neonates in the surfactant group (13% vs 73%, P = .00008). When categorized according to severity of intracranial hemorrhage and severity of bronchopulmonary dysplasia, the surfactant group was at a significant advantage (adjusted Cochran-Mantel-Haenszel X2 = 10.72, P less than .001 and X2 = 4.43, P = .036, respectively). The proportion of neonates surviving without intracranial hemorrhage and/or bronchopulmonary dysplasia was 63% in the surfactant group vs 26% in the control group (P = .0004); as for the smallest neonates, it was 58% in the surfactant group vs 4% in the control group (P = .0002). There were no differences between the groups with respect to the frequency of patent ductus arteriosus (46% vs 37%), pulmonary hemorrhage (6% vs 7%), necrotizing enterocolitis (0% vs 2%), sepsis (4% vs 2%), retinopathy of prematurity (13% vs 22%), or death (15% vs 22%). It is concluded that treatment with the single-dose surfactant regimen used in this study reduces the severity of respiratory distress during the 48 hours after treatment and decreases the major pulmonary morbidity and intracranial hemorrhage in premature neonates with RDS. Further studies are needed to determine whether (1) treatment at birth or as soon as after RDS is diagnosed and (2) the use of multiple dose of this surfactant would result in any additional benefits.

Bronchopulmonary Dysplasia↗

PubMed1996

Restoration of lung compliance with calf lung surfactant extract and a surfactant analog in an in situ model of surfactant deficiency in rats.

We have developed a standardized in situ lung surfactant deficiency model in the rat by using a single bronchoalveolar lavage (BAL). The purpose of this study was to assess the usefulness of surfactants and surfactant analogs in terms of their in vivo physiological properties. Calf lung surfactant extract (CLSE) was shown to improve lung compliance in a dose-dependent manner in this surfactant deficiency model when administered intratracheally immediately after BAL. In addition, CLSE formulated with a diether (palmityl) phosphonolipid surfactant analog significantly improved the compliance post-BAL as compared to CLSE alone. We propose that this in situ bioassay may be useful for the assessment of physiological capabilities of surfactants, surfactant analogs and surfactant formulations.

1,2-Dipalmitoylphosphatidylcholine↗

PubMed2001

Surfactant protein B deficiency: insights into surfactant function through clinical surfactant protein deficiency.

Surfactant protein B (SP-B) deficiency is a disorder of surfactant function with complete or transient absence of SP-B in term neonates. SP-B, 1 of 4 described surfactant-associated proteins, plays a key role in surfactant metabolism, particularly in intracellular packaging of surfactant components, formation of tubular myelin, and the presentation of the surfactant phospholipid monolayer to the air-fluid interface within the alveolus. Neonates with clinical SP-B deficiency best demonstrate the key role of SP-B in surfactant function. "Classic" deficiency results in severe respiratory failure in term infants and death unless lung transplantation is performed. Because the initial description of complete deficiency secondary to a homozygous frameshift mutation in codon 121 of the SP-B cDNA, partial deficiencies with differing genetic backgrounds and less severe clinical courses have been reported. These partial deficiency states may provide a clearer picture of genotype/phenotype relationships in SP-B function and surfactant metabolism. SP-B deficiency or dysfunction may be more common than once thought and may play a significant role in neonatal lung disease.

Adult↗

PubMed1996

Calcium dependent association of surfactant protein A with pulmonary surfactant: application to simple surfactant protein A purification.

Surfactant protein A (SP-A) is an abundant lipoprotein component of pulmonary surfactant that plays multiple roles in surfactant homeostasis within the lung. A simple and rapid purification procedure for SP-A is described. Purified surfactant is washed by centrifugation with Ca2+ containing buffer to remove residual soluble proteins. Following the Ca2+ buffer wash, the surfactant pellet is washed in buffer containing EGTA and Mg2+ which releases the bound SP-A in almost pure form. Subsequent chromatography of the SP-A on Sephacryl S-500 yields homogeneous preparations of the protein. The SP-A purified using this procedure requires no exposure to either detergents or organic solvents to remove lipid. SP-A prepared by this new method inhibits lipid secretion from alveolar type II cells as effectively as SP-A prepared by other methods. In addition, the SP-A depleted surfactant produced in the first step of this procedure is capable of binding exogenous SP-A in a time dependent, saturable and Ca2+ dependent manner.

Animals↗

PubMed1999

Surfactant subtype conversion is related to loss of surfactant apoprotein B and surface activity in large surfactant aggregates. Experimental and clinical studies.

Conversion of the highly surface-active subtype of pulmonary surfactant known as large surfactant aggregates (LA) to small aggregates (SA) with poor surface activity has recently been shown to occur upon cyclic changes of the air-liquid interface area in vitro. By subjecting pooled rabbit bronchoalveolar lavage fluid (BALF) to this maneuver, we found that conversion of LA to SA was accompanied by a marked decline in the ability of the remaining LA fraction to reduce surface tension by adsorption and during film compression on a pulsating bubble surfactometer. SA obtained by centrifugation of noncycled rabbit BALF had a similar phospholipid (PL) but different neutral lipid (NL) composition than did the LA. Upon cycling, the increased formation of SA obliterated this difference. No substantial difference in the PL, NL, or fatty acid profile of LA was noted before and after cycling. In contrast, the content of surfactant apoprotein-B (SP-B) in the LA decreased dramatically to nearly undetectable levels during the cycling maneuver, and this decline in SP-B content was closely correlated with the decrease in proportional appearance of LA and loss of surface activity of this fraction. Reconstitution of LA with intact SP-B after cycling virtually fully restored the surface activity of this surfactant subtype. When comparing lavage samples from adults with acute respiratory distress syndrome (ARDS; n = 10) with samples from healthy controls (n = 11), we noted a marked reduction of SP-B in the LA fraction. There was a significant correlation between the SP-B content of the LA fraction and the relative percentage of LA in BALF or the lower surface activity of this surfactant subtype. We conclude that an SP-B-related loss of LA integrity and function may substantially contribute to the decline of this surfactant subtype and the loss of its surface activity during cycling in vitro and in clinical ARDS.

Adult↗

PubMed1999

Dissociation of surfactant protein B from canine surfactant large aggregates during formation of small surfactant aggregates by in vitro surface area cycling.

Pulmonary surfactant isolated by lavage can be separated into large aggregates (LA) and small aggregates (SA). Pulse labeling experiments have shown that the LA subtype is the precursor of the SA subtype. Conversion of LA to SA can be demonstrated in vitro using the technique of surface area cycling. The precise mechanisms of surfactant subtype conversion remain unknown. We have previously reported a decline in surfactant-associated protein B (SP-B) during in vitro subtype conversion of canine surfactant. This led to the hypothesis that SP-B may be degraded by a serine protease 'convertase' during cycling. The current studies used a quantitative slot-blot assay to investigate the fates of SP-A and SP-B during in vitro cycling. These studies confirmed some SP-A is present in SA, but SP-B is confirmed to LA. Conversion leads to an apparent loss of SP-B during cycling. However, SP-B can be recovered from the walls of polypropylene and Teflon tubes by washing with chloroform:methanol. Recovered SP-B migrated on non-reducing tricine gels as a single band with an apparent molecular weight of 17 kDa, corresponding to intact SP-B dimer. Reconstitution studies demonstrated that the recovered SP-B retained its surface active properties as determined on a pulsating bubble surfactometer. We conclude in vitro surface area cycling of canine LA results in the dissociation of SP-B from surfactant lipids resulting in an apparent decline in SP-B levels.

Animals↗

PubMed2005

Properties of mixed micelles of cationic gemini surfactants and nonionic surfactant triton X-100: effects of the surfactant composition and the spacer length.

The mixed micelles of cationic gemini surfactants C12C(S)C12Br2 (S=3, 6, and 12) with the nonionic surfactant Triton X-100 (TX100) have been studied by steady-state fluorescence, time-resolved fluorescence quenching, electrophoretic light scattering, and electron spin resonance. Both the surfactant composition and the spacer length are found to influence the properties of mixed micelles markedly. The total aggregation number of alkyl chains per micelle (N(T)) goes through a minimum at X(TX100)=0.8. Meanwhile, the micropolarity of the mixed micelles decreases with increasing X(TX100), while the microviscosity increases. The presence of minimum in N(T) is explained in terms of the competition of the reduction of electrostatic repulsion between headgroups of cationic gemini surfactant with the enhancement of steric repulsion between hydrophilic headgroups of TX100 caused by the addition of TX100. The variations of micropolarity and microviscosity indicate that the incorporation of TX100 to the gemini surfactants leads to a more compact and hydrophobic micellar structure. Moreover, for the C12C3C12Br2/TX100 mixed micelle containing C12C3C12Br2 with a shorter spacer, the more pronounced decrease of N(T) at X(TX100) lower than 0.8 may be attributed to the larger steric repulsion between headgroups of TX100. Meanwhile, the increase of microviscosity and the decrease of micropolarity are more marked for the C12C12C12Br2/TX100 mixed micelle, owing to the looped conformation of the longer spacer of C12C12C12Br2.

Journal Article↗

PubMed1997

Effects of pulmonary surfactant on macrophage migration: suppression of chemokinesis by surfactant phospholipid and enhancement of chemotaxis by surfactant protein.

We fractionated the bronchoalveolar lavage fluid (BALF) from normal rabbit lungs into several fractions by high speed centrifugation and ethanol-ether extraction. Random migration, chemokinesis and chemotaxis of freshly harvested alveolar macrophages (AM), 24 h cultured AM, and peritoneal exudate cells (PEC) were assayed in vitro using a modified, under agarose method and a blind well chemotactic chamber method. Freshly harvested AM demonstrated little random migration compared with PEC. However, when freshly harvested AM were pre-incubated in surfactant free medium for 24 h, the cells showed the same rate of migration as PEC. The increased migration of the 24 h cultured AM was partially suppressed by the presence of all BALF fractions containing high proportions of phospholipid. The inhibition by Fr-L (a fraction enriched in phospholipids) was reversed by normal serum, but not by heat-inactivated serum, cholesterol, synthetic dipalmitoyl phosphatidyl choline, or indomethacin. Fr-L markedly suppressed macrophage chemokinesis but did not affect on macrophage chemotaxis. Alternatively, Fr-P, a delipidated preparation of surfactant consisting mainly of protein, had no effect on macrophage chemokinesis but increased the chemotaxis of PEC to zymosan-activated serum. We conclude that surfactant phospholipid suppresses AM migration, while surfactant protein increases macrophage chemotaxis.

Animals↗

PubMed2003

Studies of mixed surfactant solutions of cationic dimeric (gemini) surfactant with nonionic surfactant C12E6 in aqueous medium.

The interaction between the alkanediyl-alpha,omega-type cationic gemini surfactant, [(C(16)H(33)N(+)(CH(3))(2)(CH(2))(4)N(+)(CH(3))(2)C(16)H(33))2Br(-)], 16-4-16 and the conventional nonionic surfactant [CH(3)(CH(2))(10)CH(2)(OCH(2)CH(2))(6)OH], C(12)E(6) in aqueous medium has been investigated. The critical micelle concentrations of different mixtures have been measured by surface tension using a du Nouy tensiometer in aqueous solution at different temperatures (303, 308, and 313 K). Maximum surface excess (Gamma(max)) and minimum area per molecule (A(min)) were evaluated from a surface tension vs log(10)C (C is concentration) plot. The cmc value of the mixture was used to compute beta(m), the interaction parameter. The beta(sigma), the interaction parameter at the monolayer air-water interface, was also calculated. We observed synergism in 16-4-16/C(12)E(6) system at all concentration ratios. The micelle aggregation number (N(agg)) has been measured using a steady state fluorescence quenching method at a total surfactant concentration approximately 2 mM at 25 degrees C. The micropolarity and the binding constant (K(sv)) of mixed systems were determined from the ratio of intensity of peaks (I(1)/I(3)) of the pyrene fluorescence emission spectrum. The micellar interiors were found to be reasonably polar. We also found, using Maeda's concept, that the chain-chain interactions are very important in this system.

Journal Article↗