Minimal surface tension, squeeze-out and transition temperatures of binary mixtures of dipalmitoylphosphatidylcholine and unsaturated phospholipids

Egberts, J.; Sloot, H.J.; Mazure, A.

doi:10.1016/0005-2760(89)90072-6

Cited by 40 publications

(24 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Then, the surfactant monolayer phase becomes heterogenous, associating a gel and liquid state. Indeed, the T m of DPPC is 41ЊC, but, in the presence of phosphatidylglycerol and unsaturated lipids, the apparent T m of the lipid mixture is shifted down to 37ЊC (45,46). On artificial phospholipid substrates, this microheterogeneity was reported to enhance greatly the interfacial recognition with sPLA2, therefore increasing the catalytic activity (47).…”

Section: Discussionmentioning

confidence: 98%

Generation of lyso-phospholipids from surfactant in acute lung injury is mediated by type-II phospholipase A2 and inhibited by a direct surfactant protein A-phospholipase A2 protein interaction.

Arbibe¹,

Koumanov²,

Vial³

et al. 1998

J. Clin. Invest.

170

144

View full text Add to dashboard Cite

Lyso-phospholipids exert a major injurious effect on lung cell membranes during Acute Respiratory Distress Syndrome (ARDS), but the mechanisms leading to their in vivo generation are still unknown. Intratracheal administration of LPS to guinea pigs induced the secretion of type II secretory phospholipase A2 (sPLA2-II) accompanied by a marked increase in fatty acid and lyso-phosphatidylcholine (lyso-PC) levels in the bronchoalveolar lavage fluid (BALF). Administration of LY311727, a specific sPLA2-II inhibitor, reduced by 60% the mass of free fatty acid and lyso-PC content in BALF. Gas chromatography/mass spectrometry analysis revealed that palmitic acid and palmitoyl-2-lyso-PC were the predominant lipid derivatives released in BALF. A similar pattern was observed after the intratracheal administration of recombinant guinea pig (r-GP) sPLA2-II and was accompanied by a 50-60% loss of surfactant phospholipid content, suggesting that surfactant is a major lung target of sPLA2-II. In confirmation, r-GP sPLA2-II was able to hydrolyze surfactant phospholipids in vitro. This hydrolysis was inhibited by surfactant protein A (SP-A) through a direct and selective protein-protein interaction between SP-A and sPLA2-II. Hence, our study reports an in vivo direct causal relationship between sPLA2-II and early surfactant degradation and a new process of regulation for sPLA2-II activity. Anti-sPLA2-II strategy may represent a novel therapeutic approach in lung injury, such as ARDS. (

show abstract

Section: Discussionmentioning

confidence: 98%

Generation of lyso-phospholipids from surfactant in acute lung injury is mediated by type-II phospholipase A2 and inhibited by a direct surfactant protein A-phospholipase A2 protein interaction.

Arbibe¹,

Koumanov²,

Vial³

et al. 1998

J. Clin. Invest.

170

144

View full text Add to dashboard Cite

show abstract

“…PC16:0/16:0 is essential in pulmonary surfactant to oppose surface tension forces at the air-liquid interface in the lungs (17). This function is dependent on the high gel to sol phase transition temperature (41~ of PC16:0/I 6:0 which, consequently, is an inert solid material at body temperature (18). Pulmonary surfactant contains specialized unsaturated phosphatidylglycerol and specific apoprotein components designed to facilitate adsorption of this solid PC 16:0/16:0 to the air-liquid interface (17,18).…”

Section: Discussionmentioning

confidence: 99%

“…This function is dependent on the high gel to sol phase transition temperature (41~ of PC16:0/I 6:0 which, consequently, is an inert solid material at body temperature (18). Pulmonary surfactant contains specialized unsaturated phosphatidylglycerol and specific apoprotein components designed to facilitate adsorption of this solid PC 16:0/16:0 to the air-liquid interface (17,18). These constraints imposed on pulmonary surfactant by the saturated nature of PCI6:0/16:0 will not apply to gastric surfactant, as this is composed principally of the more fluid molecules PCI6:0/18:1 and PC I 6:0/18:2.…”

Section: Discussionmentioning

confidence: 99%

Rat gastric hydrophobic barrier: Modulation of phosphatidylcholine molecular species by dietary lipids

Bernhard

Postle

Linck

et al. 1996

Lipids

View full text Add to dashboard Cite

Phospholipids protect the gastric mucosa by forming a proton-repellent hydrophobic layer on its luminal surface. We have recently shown that two molecular species of phosphatidylcholine (PC), PC16:0/18:1, and PC16:0/18:2, but not PC16:0/16:0, are predominantly released into gastric mucus. We investigated whether these molecular species in mucus are modified by dietary fat. Rats were fed (for three weeks) a diet supplemented with either 10% cod liver, palm, or sunflower oil, or 10% corn starch as a control. In tissue, cod liver oil decreased PC16:0/20:4 and PC18:0/20:4. Cod liver oil and palm oil increased PC16:0/18:1, whereas sunflower oil decreased PC16:0/18:1. Palm oil additionally decreased PC16:0/18:2, whereas the other diets had no effect on PC16:0/18:2. In mucus, however, PC16:0/18:1 and PC16:0/18:2 were not significantly altered by any diet. They were increased over tissue values and comprised 37.6 +/- 3.3 and 33.1 +/- 1.4 mol% in controls. PC16:0/16:0 was lower in mucus than in mucosa and even decreased by cod liver oil (1.2 +/- 0.2 vs. 2.7 +/- 0.3 mol%; P < 0.01). We conclude that PC16:0/18:1 and PC16:0/18:2 are modified by dietary fat in tissue. In gastric secretions, however, PC16:0/18:1 and PC16:0/18:2 are kept constant and together comprise 70 mol% of the released PC species, whereas PC16:0/16:0 does not play a role for the gastric hydrophobic barrier under any dietary treatment. Additionally, cod liver oil decreases the content of PC16:0/20:4 and PC18:0/20:4 in gastric mucosa, thereby possibly decreasing the formation of eicosanoids.

show abstract

“…These changes in minimal surface pull are firstly the effect of preferential squeeze-out of unsaturated phospholipids and later on of losses of saturated PC from the monolayer [13].…”

Section: Discussionmentioning

confidence: 99%

Postmortem Effects on the Yield and Composition of Alveolar Surfactant from Rat Lungs

Egberts

Sietaram²

1990

Respiration

Self Cite

View full text Add to dashboard Cite

Isolation of alveolar surfactant from human cadaver lungs might be ineffective because of postmortem effects. We studied therefore in the rat the effect of autolysis on the yield and composition of alveolar surfactant at different intervals after death. The total amount of phospholipids in the lavage fluids decreased at 4 h postmortem and increased thereafter again. Increased amounts of proteins, significant deviations from the normal phospholipid composition of surfactant and decreased surface activity were already present from 2 h onwards. However, a normal alveolar surfactant can be obtained up to 16 h after death by using a sucrose gradient centrifugation procedure. With this procedure it is possible to isolate a surfactant with adequate surface activity from mildly, but not from severely autolytic rat lungs

show abstract

Minimal surface tension, squeeze-out and transition temperatures of binary mixtures of dipalmitoylphosphatidylcholine and unsaturated phospholipids

Cited by 40 publications

References 28 publications

Generation of lyso-phospholipids from surfactant in acute lung injury is mediated by type-II phospholipase A2 and inhibited by a direct surfactant protein A-phospholipase A2 protein interaction.

Generation of lyso-phospholipids from surfactant in acute lung injury is mediated by type-II phospholipase A2 and inhibited by a direct surfactant protein A-phospholipase A2 protein interaction.

Rat gastric hydrophobic barrier: Modulation of phosphatidylcholine molecular species by dietary lipids

Postmortem Effects on the Yield and Composition of Alveolar Surfactant from Rat Lungs

Contact Info

Product

Resources

About