The Surfactant System of the Lung

Rooney, Seamus A.

doi:10.1007/978-3-642-69521-6_15

Cited by 4 publications

(4 citation statements)

References 214 publications

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“…Turnover studies with different labeled surfacrant phospholipids after secretion have demonstrated half-lives of between 15 and 30 h [60,155]. The fate of secreted surfactant material seems to be determined by five mechanisms: -Intraalveolar catabolism -Phagocytosis and degradation by alveolar macrophages [110,118] -Removal by the mucociliary escalator -Recycling into the alveolar type II cell -Redistribution into other surrounding tissue Clearance studies in rabbits [140] have shown that approximately 7% of radiolabeled phosphatidylcholine is removed via the upper airways in 24 h, suggesting that this pathway is only of minor importance.…”

Section: Synthesis Regulation and Metabolismmentioning

confidence: 99%

The surfactant system of the adult lung: physiology and clinical perspectives

1992

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Pulmonary surfactant is synthesized and secreted by alveolar type II cells and constitutes an important component of the alveolar lining fluid. It comprises a unique mixture of phospholipids and surfactant-specific proteins. More than 30 years after its first biochemical characterization, knowledge of the composition and functions of the surfactant complex has grown considerably. Its classically known role is to decrease surface tension in alveolar air spaces to a degree that facilitates adequate ventilation of the peripheral lung. More recently, other important surfactant functions have come into view. Probably most notable among these, surfactant has been demonstrated to enhance local pulmonary defense mechanisms and to modulate immune responses in the alveolar milieu. These findings have prompted interest in the role and the possible alterations of the surfactant system in a variety of lung diseases and in environmental impacts on the lung. However, only a limited number of studies investigating surfactant changes in human lung disease have hitherto been published. Preliminary results suggest that surfactant analyses, e.g., from bronchoalveolar lavage fluids, may reveal quantitative and qualitative abnormalities of the surfactant system in human lung disorders. It is hypothesized that in the future, surfactant studies may become one of our clinical tools to evaluate the activity and severity of peripheral lung diseases. In certain disorders they may also gain diagnostic significance. Further clinical studies will be necessary to investigate the potential therapeutic benefits of surfactant substitution and the usefulness of pharmacologic manipulation of the secretory activity of alveolar type II cells in pulmonary medicine.

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Section: Synthesis Regulation and Metabolismmentioning

confidence: 99%

The surfactant system of the adult lung: physiology and clinical perspectives

1992

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“…The neuroen docrine effect is believed to occur through the placental transfer of TRH and stimulation of the fetal pituitary-thyroid axis leading to an increase in fetal plasma TH concentration [1,18,19], TH are known to accelerate fetal lung development [35,36], The neurotransmitter effect of TRH is mediated by the stimulation of fetal CNS sympathetic or parasympathetic activity [1]. The lack of a suitable animal model has hampered study of the mechanism of TRH-mediated fetal lung maturation.…”

Section: Discussionmentioning

confidence: 99%

Fetal Mouse Lung Ultrastructural Maturation Is Accelerated by Maternal Thyrotropin-Releasing Hormone Treatment

et al. 1996

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Maternal administration of thyrotropin-releasing hormone, alone or in combination with corticosteroid, accelerates functional, morphologic and biochemical fetal lung maturation. However, the dose-response relationship of maternal thyrotropin-releasing hormone treatment and acceleration of fetal lung ultrastructural maturation or disaturated phosphatidylcholine content has not been investigated. We administered (i.p.) saline or thyrotropin-releasing hormone (0.2, 0.4 or 0.6 mg/kg/dose) to the pregnant Balb/c mouse on days 16 and 17 (b.i.d.) and on day 18 of gestation (1 h prior to killing). Morphometric ultrastructural analysis and quantitation of disaturated phosphatidylcholine content was done on the 18-day gestation fetal lung. Maternal thyrotropin-releasing hormone treatment resulted in an increase in the number of lamellar bodies and depletion of glycogen in fetal lung type II cells, and an increase in the lung airspace to parenchymal ratio. In addition, a striking difference in the pattern of lung growth was noted in the thyrotropin-releasing-hormone-treated (0.4 and 0.6 mg/kg/dose) groups. These lungs had larger air spaces, thinner alveolar septae and more air-blood barriers. Maternal thyrotropin-releasing hormone treatment did not influence fetal lung disaturated phosphatidylcholine content. We conclude that in the mouse, maternal thyrotropin-releasing hormone treatment enhances fetal lung structural maturation and propose that thyrotropin-releasing hormone plays a role in mammalian fetal lung growth.

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“…Surfactant proteins can be divided into the hydrophobic proteins SP-B and SP-C and the hydrophilic proteins SP-A and SP-D. While SP-A and SP-D play essential roles in the pulmonary immune defense, SP-B and SP-C lower the surface-tension and facilitate formation and stabilization of the surfactant film [19,20]. …”

Section: Reviewmentioning

confidence: 99%

Interstitial lung disease in children – genetic background and associated phenotypes

Hartl

Griese

2005

Respir Res

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Interstitial lung disease in children represents a group of rare chronic respiratory disorders. There is growing evidence that mutations in the surfactant protein C gene play a role in the pathogenesis of certain forms of pediatric interstitial lung disease. Recently, mutations in the ABCA3 transporter were found as an underlying cause of fatal respiratory failure in neonates without surfactant protein B deficiency. Especially in familiar cases or in children of consanguineous parents, genetic diagnosis provides an useful tool to identify the underlying etiology of interstitial lung disease. The aim of this review is to summarize and to describe in detail the clinical features of hereditary interstitial lung disease in children. The knowledge of gene variants and associated phenotypes is crucial to identify relevant patients in clinical practice.

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The Surfactant System of the Lung

Cited by 4 publications

References 214 publications

The surfactant system of the adult lung: physiology and clinical perspectives

The surfactant system of the adult lung: physiology and clinical perspectives

Fetal Mouse Lung Ultrastructural Maturation Is Accelerated by Maternal Thyrotropin-Releasing Hormone Treatment

Interstitial lung disease in children – genetic background and associated phenotypes

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