Impaired recycling of surfactant-like liposomes in type II pneumocytes from injured lungs

Müller, Bernd; Garn, Holger; Hochscheid, Renate

doi:10.1136/thorax.58.2.127

Cited by 9 publications

(5 citation statements)

References 30 publications

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“…Furthermore, it is difficult to determine if this decreased recycling is a primary or secondary factor in these infants' continuing need for mechanical ventilation resulting from alveolar type 2 cell dysfunction. 26 Alternatively, it may not be a matter of decreased surfactant recycling but rather improved substrate availability and utilization as well as maturity of type 2 cells that promote new surfactant synthesis with less reliance on recycled phospholipids. Fat and total caloric intake increased with age in our study population.…”

Section: Discussionmentioning

confidence: 99%

Substrate utilization and kinetics of surfactant metabolism in evolving bronchopulmonary dysplasia

Spence

Zozobrado²,

Patterson³

et al. 2005

The Journal of Pediatrics

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Section: Discussionmentioning

confidence: 99%

Substrate utilization and kinetics of surfactant metabolism in evolving bronchopulmonary dysplasia

Spence

Zozobrado²,

Patterson³

et al. 2005

The Journal of Pediatrics

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“…Further, data represent that EVALI is more predominant in young people. 12 Due to the highly efficient recycling of surfactant in young 69 and injured 70 lungs, EVALI persistence is thereby exacerbated.…”

Section: ■ Discussionmentioning

confidence: 99%

A Mechanical Mechanism for Vitamin E Acetate in E-cigarette/Vaping-Associated Lung Injury

DiPasquale¹,

Gbadamosi²,

Nguyen³

et al. 2020

Chem. Res. Toxicol.

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The outbreak of electronic-cigarette/vaping-associated lung injury (EVALI) has made thousands ill. This lung injury has been attributed to a physical interaction between toxicants from the vaping solution and the pulmonary surfactant. In particular, studies have implicated vitamin E acetate as a potential instigator of EVALI. Pulmonary surfactant is vital to proper respiration through the mechanical processes of adsorption and interface stability to achieve and maintain low surface tension at the air−liquid interface. Using neutron spin echo spectroscopy, we investigate the impact of vitamin E acetate on the mechanical properties of two lipid-only pulmonary surfactant mimics: pure 1,2-dipalmitoyl-sn-glycero-3-phosphocholine and a more comprehensive lipid mixture. It was found that increasing vitamin E acetate concentration nonlinearly increased membrane fluidity and area compressibility to a plateau. Softer membranes would promote adsorption to the air−liquid interface during inspiration as well as collapse from the interface during expiration. These findings indicate the potential for the failure of the pulmonary surfactant upon expiration, attributed to monolayer collapse. This collapse could contribute to the observed EVALI signs and symptoms, including shortness of breath and pneumonitis.

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“…Increased surfactant levels may be due to an augmented synthesis and/or impaired endocytosis of surfactant by type II cells, which might occur when type II cell membranes are damaged or when plasma proteins are present in the alveolar space. Pulmonary surfactant has a crucial role in the normal physiology of the lungs [ 47 ], and our data suggest that the intrinsic activity of pulmonary surfactant may be significantly decreased during murine MA-ALI/ARDS [ 47 , 48 ]. In fact in the Pb NK65-infected mice, vascular leakage and pulmonary oedema result in increased protein levels, either in the total BAL supernatant or in the BAL LA fraction.…”

Section: Discussionmentioning

confidence: 99%

Altered Lipid Composition of Surfactant and Lung Tissue in Murine Experimental Malaria-Associated Acute Respiratory Distress Syndrome

et al. 2015

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Malaria-associated acute lung injury (MA-ALI) and its more severe form malaria-associated acute respiratory distress syndrome (MA-ARDS) are common, often fatal complications of severe malaria infections. However, little is known about their pathogenesis. In this study, biochemical alterations of the lipid composition of the lungs were investigated as possible contributing factors to the severity of murine MA-ALI/ARDS. C57BL/6J mice were infected with Plasmodium berghei NK65 to induce lethal MA-ARDS, or with Plasmodium chabaudi AS, a parasite strain that does not induce lung pathology. The lipid profile of the lung tissue from mice infected with Plasmodium berghei NK65 developing MA-ALI/ARDS, but not that from mice without lung pathology or controls, was characterized by high levels of phospholipids -mainly phosphatidylcholine- and esterified cholesterol. The high levels of polyunsaturated fatty acids and the linoleic/oleic fatty acid ratio of the latter reflect the fatty acid composition of plasma cholesterol esters. In spite of the increased total polyunsaturated fatty acid pool, which augments the relative oxidability of the lung membranes, and the presence of hemozoin, a known pro-oxidant, no excess oxidative stress was detected in the lungs of Plasmodium berghei NK65 infected mice. The bronchoalveolar lavage (BAL) fluid of Plasmodium berghei NK65 infected mice was characterized by high levels of plasma proteins. The phospholipid profile of BAL large and small aggregate fractions was also different from uninfected controls, with a significant increase in the amounts of sphingomyelin and lysophosphatidylcholine and the decrease in phosphatidylglycerol. Both the increase of proteins and lysophosphatidylcholine are known to decrease the intrinsic surface activity of surfactant. Together, these data indicate that an altered lipid composition of lung tissue and BAL fluid, partially ascribed to oedema and lipoprotein infiltration, is a characteristic feature of murine MA-ALI/ARDS and possibly contribute to lung dysfunction.

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Impaired recycling of surfactant-like liposomes in type II pneumocytes from injured lungs

Cited by 9 publications

References 30 publications

Substrate utilization and kinetics of surfactant metabolism in evolving bronchopulmonary dysplasia

Substrate utilization and kinetics of surfactant metabolism in evolving bronchopulmonary dysplasia

A Mechanical Mechanism for Vitamin E Acetate in E-cigarette/Vaping-Associated Lung Injury

Altered Lipid Composition of Surfactant and Lung Tissue in Murine Experimental Malaria-Associated Acute Respiratory Distress Syndrome

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