On the Formation of Discoidal versus Threadlike Micelles in Dilute Aqueous Surfactant/Lipid Systems

Langmuir ◽  
2008 ◽  
Vol 24 (5) ◽  
pp. 1731-1739 ◽  
Author(s):  
Emma Johansson ◽  
Maria C. Sandström ◽  
Magnus Bergström ◽  
Katarina Edwards
2002 ◽  
Vol 282 (4) ◽  
pp. L735-L742 ◽  
Author(s):  
James L. Carroll ◽  
Diann M. McCoy ◽  
Stephen E. McGowan ◽  
Ronald G. Salome ◽  
Alan J. Ryan ◽  
...  

Tumor necrosis factor (TNF)-α is a major cytokine implicated in inducing acute and chronic lung injury, conditions associated with surfactant phosphatidylcholine (PtdCho) deficiency. Acutely, TNF-α decreases PtdCho synthesis but stimulates surfactant secretion. To investigate chronic effects of TNF-α, we investigated PtdCho metabolism in a murine transgenic model exhibiting lung-specific TNF-α overexpression. Compared with controls, TNF-α transgenic mice exhibited a discordant pattern of PtdCho metabolism, with a decrease in PtdCho and disaturated PtdCho (DSPtdCho) content in the lung, but increased levels in alveolar lavage. Transgenics had lower activities and increased immunoreactive levels of cytidylyltransferase (CCT), a key PtdCho biosynthetic enzyme. Ceramide, a CCT inhibitor, was elevated, and linoleic acid, a CCT activator, was decreased in transgenics. Radiolabeling studies revealed that alveolar reuptake of DSPtdCho was significantly decreased in transgenic mice. These observations suggest that chronic expression of TNF-α results in a complex pattern of PtdCho metabolism where elevated lavage PtdCho may originate from alveolar inflammatory cells, decreased surfactant reuptake, or altered surfactant secretion. Reduced parenchymal PtdCho synthesis appears to be attributed to CCT enzyme that is physiologically inactivated by ceramide or by diminished availability of activating lipids.


2020 ◽  
Vol 69 (24) ◽  
pp. 248701
Author(s):  
Ying Yang ◽  
◽  
Jun-Jie Song ◽  
Ming-Wei Wan ◽  
Liang-Hui Gao ◽  
...  

2000 ◽  
Vol 278 (1) ◽  
pp. L75-L80 ◽  
Author(s):  
Machiko Ikegami ◽  
Jeffrey A. Whitsett ◽  
Zissis C. Chroneos ◽  
Gary F. Ross ◽  
Jacquelyn A. Reed ◽  
...  

Mice that express interleukin (IL)-4 in Clara cells (CCSP-IL-4) develop chronic airway inflammation and an alveolar proteinosis-like syndrome. To identify the role of IL-4 in surfactant homeostasis, we measured lipid and protein metabolism in the lungs of CCSP-IL-4 mice in vivo. Alveolar saturated phosphatidylcholine (Sat PC) pools were increased 6.5-fold and lung tissue Sat PC pools were increased 4.8-fold in the IL-4 transgenic mice. Whereas surfactant protein (SP) A was increased proportionately to Sat PC, SP-D was increased approximately 90-fold in the IL-4 mice compared with wild-type mice and was associated with 2.8-fold increase in SP-D mRNA. The incorporation of palmitate and choline into Sat PC was increased about twofold in CCSP-IL-4 mice. Although trace doses of radiolabeled Sat PC were cleared from the air spaces and lungs of CCSP-IL-4 mice more slowly than in wild-type mice, net clearance of Sat PC from the lungs of CCSP-IL-4 mice was sixfold higher in the IL-4 mice than in wild-type mice because of the larger Sat PC pool sizes. Expression of IL-4 in Clara cells increased surfactant lipid synthesis and clearance, establishing a new equilibrium with increased surfactant pools and an alveolar proteinosis associated with a selective increase in SP-D protein, demonstrating a previously unexpected effect of IL-4 in pulmonary surfactant homeostasis.


1991 ◽  
Vol 260 (6) ◽  
pp. L562-L570 ◽  
Author(s):  
S. H. Randell ◽  
R. Silbajoris ◽  
S. L. Young

During the last stages of intrauterine growth, remarkable changes occur in the alveolar epithelium that include cellular differentiation and increased production of surfactant lipid and apoprotein. We made morphometric measurements of type II cell characteristics from rats aged gestational day 20 to 14 days postnatal. We also measured the amounts of disaturated phosphatidylcholine (DSPC) and surfactant apoprotein (SP-A) in lung tissue, bronchoalveolar lavage, and a lamellar body-rich fraction, and we estimated the lung content of mRNAs for SP-A, SP-B, and SP-C. Lavage and lamellar body surfactant lipid and apoprotein content per lung showed a pattern of a sharp rise in the early postnatal period, then a substantial decline, and a second increase by day 14. When normalized for dry lung weight, the highest DSPC values were found on postnatal day 1 in all compartments. The fraction of whole lung DSPC found in lamellar body or lavage was greatest in the 48-h period surrounding birth. Lamellar body SP-A was greater than lavage SP-A on gestational day 22, but a day later the lavage SP-A was 16 times greater than the lamellar body SP-A. The lung tissue content of all three apoprotein mRNAs increased sharply before birth, fell during the 1st postnatal wk, and then rose again to adult levels. Type II cell number and lamellar body number per milligram of dry lung tissue was highest on post-natal day 1 and fell by one-half during the 1st postnatal wk. The amount of DSPC per unit of lamellar body volume rose to its greatest value on postnatal day 1 and then decreased more than threefold. These findings indicate a pattern of expansion of surfactant cellular and biochemical pools at the time of birth in the rat.


1999 ◽  
Vol 83 (11) ◽  
pp. 2278-2281 ◽  
Author(s):  
Martin In ◽  
Gregory G. Warr ◽  
Raoul Zana
Keyword(s):  

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