Regulation of Surfactant Metabolism: Degradation of Internalized Alveolar Phosphatidylcholine

2015 ◽  
pp. 74-83 ◽  
Author(s):  
Aron B. Fisher ◽  
Chandra Dodia
Keyword(s):  
Surfactant Metabolism

Abnormal Surfactant Metabolism and Function in Preterm Ventilated Baboons

1998 ◽  
Vol 158 (6) ◽  
pp. 1982-1989 ◽  
Author(s):  
STEVEN R. SEIDNER ◽  
ALAN H. JOBE ◽  
JACQUELINE J. COALSON ◽  
MACHIKO IKEGAMI
Keyword(s):  
And Function ◽  
Surfactant Metabolism

Surfactant metabolism in transgenic mice after granulocyte macrophage-colony stimulating factor ablation

1996 ◽  
Vol 270 (4) ◽  
pp. L650-L658 ◽  
Author(s):  
M. Ikegami ◽  
T. Ueda ◽  
W. Hull ◽  
J. A. Whitsett ◽  
R. C. Mulligan ◽  
...  
Keyword(s):  
Protein A ◽  
Surfactant Protein ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
And Function ◽  
Stimulating Factor ◽  
Deficient Mice ◽  
Surfactant Metabolism

Mice made granulocyte macrophage-colony stimulating factor (GM-CSF)-deficient by homologous recombination maintain normal steady-state hematopoiesis but have an alveolar accumulation of surfactant lipids and protein that is similar to pulmonary alveolar proteinosis in humans. We asked how GM-CSF deficiency alters surfactant metabolism and function in mice. Alveolar and lung tissue saturated phosphatidylcholine (Sat PC) were increased six- to eightfold in 7- to 9-wk-old GM-CSF-deficient mice relative to controls. Incorporation of radiolabeled palmitate and choline into Sat PC was higher in GM-CSF deficient mice than control mice, and no loss of labeled Sat PC occurred from the lungs of GM-CSF-deficient mice. Secretion of radiolabeled Sat PC to the alveolus was similar in GM-CSF-deficient and control mice. Labeled Sat PC and surfactant protein A (SP-A) given by tracheal instillation were cleared rapidly in control mice, but there was no measurable loss from the lungs of GM-CSF-deficient mice. The function of the surfactant from GM-CSF-deficient mice was normal when tested in preterm surfactant-deficient rabbits. GM-CSF deficiency results in a catabolic defect for Sat PC and SP-A.

Surfactant metabolism in surfactant protein A-deficient mice

1997 ◽  
Vol 272 (3) ◽  
pp. L479-L485 ◽  
Author(s):  
M. Ikegami ◽  
T. R. Korfhagen ◽  
M. D. Bruno ◽  
J. A. Whitsett ◽  
A. H. Jobe
Keyword(s):  
Lung Tissue ◽  
Protein A ◽  
Surfactant Protein ◽  
Normal Lung ◽  
Tissue Slices ◽  
Normal Lung Function ◽  
Deficient Mice ◽  
Surfactant Metabolism

In the present study we asked if surfactant metabolism was altered in surfactant protein (SP) A-deficient mice in vivo. Although previous studies in vitro demonstrated that SP-A modulates surfactant secretion and reuptake by type II cells, mice made SP-A deficient by homologous recombination grow and reproduce normally and have normal lung function. Alveolar and lung tissue saturated phophatidylcholine (Sat PC) pools were 50 and 26% larger, respectively, in SP-A(-/-) mice than in SP-A(+/+) mice. Radiolabeled choline and palmitate incorporation into lung Sat PC was similar both in vivo and for lung tissue slices in vitro from SP-A(+/+) and SP-A(-/-) mice. Percent secretion of radiolabeled Sat PC was unchanged from 3 to 15 h, although SP-A(-/-) mice retained more labeled Sat PC in the alveolar lavages at 48 h (consistent with the increased surfactant pool sizes). Clearance of radiolabeled dipalmitoylphosphatidylcholine and SP-B from the air spaces after intratracheal injection was similar in SP-A(-/-) and SP-A(+/+) mice. Lack of SP-A had minimal effects on the overall metabolism of Sat PC or SP-B in mice.

scholarly journals Surfactant metabolic consequences of overexpression of GM-CSF in the epithelium of GM-CSF-deficient mice

1997 ◽  
Vol 273 (4) ◽  
pp. L709-L714 ◽  
Author(s):  
Machiko Ikegami ◽  
Alan H. Jobe ◽  
Jacquelyn A. Huffman Reed ◽  
Jeffrey A. Whitsett
Keyword(s):  
Lung Tissue ◽  
Surfactant Protein ◽  
Type Ii ◽  
Cell Numbers ◽  
Gm Csf ◽  
Type Ii Cell ◽  
Macrophage Colony ◽  
Respiratory Epithelial ◽  
Deficient Mice ◽  
Surfactant Metabolism

Granulocyte macrophage colony-stimulating factor (GM-CSF) is a regulator of surfactant metabolism because GM-CSF-deficient mice have abnormally slow clearance and catabolism of saturated phosphatidylcholine (Sat PC) and surfactant protein (SP)-A in airspaces and lung tissue. Overexpression of GM-CSF only in respiratory epithelial cells of mice deficient in GM-CSF using the SP-C promotor (GM−/−,SP-C-GM+/+) resulted in increased type II cell numbers and normalization of alveolar Sat PC pool sizes. Metabolic measurements demonstrated that incorporation of radiolabeled choline and palmitate was increased more than twofold, but the amount of radiolabeled Sat PC that accumulated in airspaces relative to the amount incorporated was decreased by 50% relative to normal GM+/+ mice. The clearance of dipalmitoylphosphatidylcholine and SP-B from the airspaces was more rapid for GM−/−,SP-C-GM+/+ mice than for GM+/+ mice. Loss of Sat PC and SP-B from the lungs (alveolar plus lung tissue) was similar in the two strains of mice. The normal surfactant pools in the GM−/−,SP-C-GM+/+ mice were achieved by the net effects of increases in type II cell numbers, increased incorporation, decreased accumulation, and increased reuptake rates for surfactant components, demonstrating the multiple effects of GM-CSF on surfactant metabolism.

Surfactant metabolism of newborn lamb lungs studied in vivo

1980 ◽  
Vol 49 (6) ◽  
pp. 1091-1098 ◽  
Author(s):  
A. Jobe ◽  
M. Ikegami ◽  
I. Sarton-Miller ◽  
L. Barajas
Keyword(s):  
Palmitic Acid ◽  
Intravenous Injection ◽  
Half Life ◽  
Lamellar Body ◽  
Lung Parenchyma ◽  
Newborn Lamb ◽  
Specific Activities ◽  
Life Values ◽  
Surfactant Metabolism

Surfactant, microsomal, and lamellar body fractions were isolated from the lungs of 5-day-old lambs 0.21-55 h after the intravenous injection of radiolabeled palmitic acid. The specific activities as cpm/mumol phospholipid phosphate of phosphatidylcholine, saturated phosphatidylcholine, phosphatidylglycerol, and phosphatidylethanolamine were measured. The palmitate-labeled phospholipids disappeared from the lung parenchyma with a half-life of approximately 50 h. The radiolabel disappeared from phosphatidylcholine, saturated phosphatidylcholine, phosphatidylglycerol, and phosphatidylethanolamine of microsomal fractions with initial half-life values of 4.5, 4.6, 1.9, and 23.9 h, respectively. The labeled phospholipids rapidly appeared in the lamellar body fraction and accumulated in the surfactant of the lambs in a linear fashion for 35 h. The curves for the labeling of surfactant with radiolabeled saturated phosphatidylcholine, phosphatidylglycerol, and phosphatidylethanolamine were similar to the curve for phosphatidylcholine.

Aspects of Surfactant Metabolism in the Adult and Perinatal Lung

1987 ◽  
pp. 183-196
Author(s):  
L. M. G. Van Golde ◽  
R. Burkhardt ◽  
A. C. J. De Vries ◽  
J. J. Batenburg
Keyword(s):  
Surfactant Metabolism

Localization of a candidate surfactant convertase to type II cells, macrophages, and surfactant subfractions

1999 ◽  
Vol 276 (3) ◽  
pp. L452-L458 ◽  
Author(s):  
Howard Clark ◽  
Lennell Allen ◽  
Erin Collins ◽  
Frederick Barr ◽  
Leland Dobbs ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Alveolar Macrophages ◽  
Pulmonary Surfactant ◽  
Type Ii Cells ◽  
Type Ii ◽  
Clara Cells ◽  
Rat Lung ◽  
Protein Distribution ◽  
Serine Hydrolase ◽  
Surfactant Metabolism

Pulmonary surfactant exists in the alveolus in several distinct subtypes that differ in their morphology, composition, and surface activity. Experiments by others have implicated a serine hydrolase in the production of the inactive small vesicular subtype of surfactant (N. J. Gross and R. M. Schultz. Biochim. Biophys. Acta 1044: 222–230, 1990). Our laboratory recently identified this enzyme in the rat as the serine carboxylesterase ES-2 [F. Barr, H. Clark, and S. Hawgood. Am. J. Physiol. 274 ( Lung Cell. Mol. Physiol. 18): L404–L410, 1998]. In the present study, we determined the cellular sites of expression of ES-2 in rat lung using a digoxygenin-labeled ES-2 riboprobe. ES-2 mRNA was localized to type II cells and alveolar macrophages but not to Clara cells. Using a specific ES-2 antibody, we determined the protein distribution of ES-2 in the lung by immunohistochemistry, and it was found to be consistent with the sites of mRNA expression. Most of the ES-2 in rat bronchoalveolar lavage is in the surfactant-depleted supernatant, but ES-2 was also consistently localized to the small vesicular surfactant subfraction presumed to form as a consequence of conversion activity. These results are consistent with a role for endogenous lung ES-2 in surfactant metabolism.

Surfactant treatments alter endogenous surfactant metabolism in rabbit lungs

1990 ◽  
Vol 68 (4) ◽  
pp. 1590-1596 ◽  
Author(s):  
S. B. Oetomo ◽  
J. Lewis ◽  
M. Ikegami ◽  
A. H. Jobe
Keyword(s):  
Lower Lobe ◽  
Left Lower Lobe ◽  
Exogenous Surfactant ◽  
Main Stem Bronchus ◽  
Label Incorporation ◽  
Left Main Stem Bronchus ◽  
The Right ◽  
Surfactant Metabolism

The effect of exogenous surfactant on endogenous surfactant metabolism was evaluated using a single-lobe treatment strategy to compare effects of treated with untreated lung within the same rabbit. Natural rabbit surfactant, Survanta, or 0.45% NaCl was injected into the left main stem bronchus by use of a Swan-Ganz catheter. Radio-labeled palmitic acid was then given by intravascular injection at two times after surfactant treatment, and the ratios of label incorporation and secretion in the left lower lobe to label incorporation and secretion in the right lung were compared. The treatment procedure resulted in a reasonably uniform surfactant distribution and did not disrupt lobar pulmonary blood flow. Natural rabbit surfactant increased incorporation of palmitate into saturated phosphatidylcholine (Sat PC) approximately 2-fold (P less than 0.01), and secretion of labeled Sat PC increased approximately 2.5-fold in the surfactant-treated left lower lobe relative to the right lung (P less than 0.01). Although Survanta did not alter incorporation, it did increase secretion but not to the same extent as rabbit surfactant (P less than 0.01). Alteration of endogenous surfactant Sat PC metabolism in vivo by surfactant treatments was different from that which would have been predicted by previous in vitro studies.

scholarly journals Outcomes of Lung Transplantation for Infants and Children with Genetic Disorders of Surfactant Metabolism

2017 ◽  
Vol 184 ◽  
pp. 157-164.e2 ◽  
Author(s):  
Whitney B. Eldridge ◽  
Qunyuan Zhang ◽  
Albert Faro ◽  
Stuart C. Sweet ◽  
Pirooz Eghtesady ◽  
...  
Keyword(s):  
Lung Transplantation ◽  
Genetic Disorders ◽  
Infants And Children ◽  
Surfactant Metabolism
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