Influence of phosphatidylglycerol on the uptake of liposomes by alveolar cells and on lung function

Poelma, D. L. H.; Lachmann, Burkhard; Haitsma, Jack J.; Zimmermann, Luc J. I.; Iwaarden, J. Freek van

doi:10.1152/japplphysiol.01164.2004

Cited by 8 publications

(10 citation statements)

References 37 publications

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“…Surfactant lipids and proteins may subsequently become ligands for one or more of these receptors. It is also notable that phosphatidyl glycerol facilitates clearance of surfactant phospholipids by alveolar macrophages [172,173]. These studies indicate that alveolar macrophages and alveolar type II epithelial cells coordinate surfactant metabolism and innate host defense properties of pulmonary surfactant.…”

Section: Sp-b Sp-c and Surfactant Lipidsmentioning

confidence: 82%

Pulmonary Surfactant: An Immunological Perspective

Chroneos

Sever-Chroneos

Shepherd

2010

Cell Physiol Biochem

166

115

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Section: Sp-b Sp-c and Surfactant Lipidsmentioning

confidence: 82%

Pulmonary Surfactant: An Immunological Perspective

Chroneos

Sever-Chroneos

Shepherd

2010

Cell Physiol Biochem

166

115

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“…Instillation of an exogenous surfactant, Curosurf, in newborn and adult rabbits showed negligible uptake by AM after 3 h, although AM degraded Curosurf in vitro (1). In part, the variability between studies may be due to experimental conditions and the lipid composition of the material (32), suggesting that the internalization of exogenous preparations, either in vitro or in vivo, may not accurately reflect the role of AM in clearing endogenous surfactant.…”

mentioning

confidence: 99%

Alveolar macrophage depletion is associated with increased surfactant pool sizes in adult rats

Forbes¹,

Pickell²,

Foroughian³

et al. 2007

Journal of Applied Physiology

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monary surfactant is a lipid-protein material that is essential for normal lung function. Maintaining normal and consistent alveolar amounts of surfactant is in part dependent on clearance of surfactant by alveolar macrophages (AM). The present study utilized a rat model of AM depletion to determine the impact on surfactant pool sizes and function over time. Male Sprague-Dawley rats were anesthetized and intratracheally instilled with PBS-liposomes (PBS-L) or dichloromethylene diphosphonic acid (DMDP) containing liposomes (DMDP-L) and were killed at various time points up to 21 days for compliance measurements, AM cell counts, and surfactant analysis. AM numbers were significantly decreased 1, 2, and 3 days after instillation in DMDP-L vs. PBS-L, with 72% depletion at 3 days. AM numbers returned to normal levels by 5 days. In DMDP-L rats, there was a rapid increase in surfactant-phospholipid pools, showing a ninefold increase in the amount of surfactant in the lavage 3 days after liposome instillation. Surfactant accumulation progressed up to 7 days, with pools normalizing by 21 days. The increase in surfactant was due to increases in both subfractions of surfactant, the large aggregates (LA) and small aggregates. Surfactant protein A levels, relative to LA phospholipids, were not increased. There was a decreased extent of surfactant conversion in vitro for LA from DMDP-L rats compared with controls. It is concluded that the procedure of AM depletion significantly affects surfactant metabolism. The increased endogenous surfactant must be considered when utilizing the AM depletion model to study the role of these cells during lung insults. pulmonary surfactant; surfactant metabolism; dichloromethylene diphosphonic acid; pulmonary alveolar proteinosis

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“…The animals were then tracheotomized and a sterile metal cannula was inserted into the trachea. After these surgical procedures, the animals were mechanically ventilated as described [4,30,31] . After disconnection from the ventilator, the liposomes were administered intratracheally at the indicated dosage.…”

Section: Intratracheal Instillation Of Fluorescent Liposomesmentioning

confidence: 99%

“…The alveolar type II cells and alveolar macrophages were isolated as described [4,30,31] 6 cells/ml and stored on ice until further use. Alveolar macrophages were identified using monoclonal antibodies specific for rat macrophages (ED9) and alveolar type II cells were identified using an alkaline phosphatase assay as described by Edelson et al [32] .…”

Section: Isolation Of Alveolar Type II Cells and Alveolar Macrophagesmentioning

confidence: 99%

“…The mean cell-associated fluorescence was determined of all the cells, including the cells, which did not internalize the fluorescent liposomes. In addition, the mean cell-associated fluorescence was determined of the cells with a fluorescence higher then the autofluorescence (Mean cell-associated fluorescence of gated cells) as described before [4,30,31] .…”

Section: Flow Cytometrymentioning

confidence: 99%

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Effect of SP-B Peptides on the Uptake of Liposomes by Alveolar Cells

et al. 2006

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Background: Exogenous surfactant has been accepted worldwide as a therapy of RDS in premature and term infants. Exogenous surfactant is usually derived from lung extracts containing phospholipids and the surfactant proteins SP-B and SP-C. Synthetic peptides of SP-B and SP-C are being tested with the aim to develop a completely synthetic surfactant preparation. Nevertheless, the effects of these peptides on the endogenous surfactant metabolism remain unknown. Objectives: The effect of synthetic SP-B peptides on uptake of surfactant-like liposomes was investigated in alveolar cells. Native SP-B and seven SP-B peptides were included: monomeric and dimeric SP-B_1–25 (Cys-11 → Ala-11), SP-B_63–78and Ala-SP-B_63–78 (Cys-71 → Ala-71;Cys-77 → Ala-77)and their serine mutants. Methods: In vitro, alveolar macrophages (AM) and alveolar type II cells (ATII) were incubated with liposomes containing SP-B or one of its peptides. In vivo, rats received intratracheally various SP-B peptides (SP-B/lipid ratio 1:33 w/w) incorporated in fluorescent surfactant-like liposomes. One hour after instillation, AM and ATII were isolated and cell-associated fluorescence was determined using flow cytometry. Confocal laser microscopy was performed to ensure internalization of the liposomes. Results: In vitro uptake by AM or ATII was not influenced by the SP-B peptides. In vivo, SP-B_1–25 and Ser-SP-B_1–25 increased the uptake by AM whereas dSP-B_1–25 decreased the uptake. Neither SP-B_1–25 nor dSP-B_1–25affected total uptake by ATII. The overall uptake by SP-B_63–78 variants was not changed. Conclusions: Surface-active synthetic SP-B peptides do not interfere with the normaluptake of surfactant by ATII.

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Influence of phosphatidylglycerol on the uptake of liposomes by alveolar cells and on lung function

Cited by 8 publications

References 37 publications

Pulmonary Surfactant: An Immunological Perspective

Pulmonary Surfactant: An Immunological Perspective

Alveolar macrophage depletion is associated with increased surfactant pool sizes in adult rats

Effect of SP-B Peptides on the Uptake of Liposomes by Alveolar Cells

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