Properties of an acid phosphatase in pulmonary surfactant.

Benson, Bradley J.

doi:10.1073/pnas.77.2.808

Cited by 16 publications

(4 citation statements)

References 29 publications

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“…The role of acid phosphatase in microbial infections is not clear, although it is likely that this lipid phosphohydrolase has critical roles in lung morphogenesis and in acute lung injury and repair 39 . The presence of acid phosphatase has been previously described in mammalian ALF 40 , where this enzyme contains characteristics of the microsomal enzyme, and it is quite specific for the hydrolysis of phosphatidic acid and 1-acyl-2-lysophosphatidic acid. An increase of acid phosphatase in CF-ALF may correspond to the homeostatic necessity to quickly degrade accumulation of lysophospholipids, which are related to surfactant dysfunction and lung inflammation 41 .…”

Section: Discussionmentioning

confidence: 86%

Modifications of Pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells

Hill

Scordo

Arcos

et al. 2017

Sci Rep

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Pseudomonas aeruginosa is a ubiquitous environmental organism and an opportunistic pathogen that causes chronic lung infections in the airways of cystic fibrosis (CF) patients as well as other immune-compromised individuals. During infection, P. aeruginosa enters the terminal bronchioles and alveoli and comes into contact with alveolar lining fluid (ALF), which contains homeostatic and antimicrobial hydrolytic activities, termed hydrolases. These hydrolases comprise an array of lipases, glycosidases, and proteases and thus, they have the potential to modify lipids, carbohydrates and proteins on the surface of invading microbes. Here we show that hydrolase levels between human ALF from healthy and CF patients differ. CF-ALF influences the P. aeruginosa cell wall by reducing the content of one of its major polysaccharides, Psl. This CF-ALF induced Psl reduction does not alter initial bacterial attachment to surfaces but reduces biofilm formation. Importantly, exposure of P. aeruginosa to CF-ALF drives the activation of neutrophils and triggers their oxidative response; thus, defining human CF-ALF as a new innate defense mechanism to control P. aeruginosa infection, but at the same time potentially adding to the chronic inflammatory state of the lung in CF patients.

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Section: Discussionmentioning

confidence: 86%

Modifications of Pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells

Hill

Scordo

Arcos

et al. 2017

Sci Rep

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“…It has been suggested that measurement of PAPase in amniotic fluid might be used in the prediction of fetal lung maturity (142,146). PAPase has also been reported to be associated with surfactant in the dog lung (147). The relationship, if any, between the PAPase associated with surfactant and that involved in the synthesis of lung phospholipids, including surfactant, is not known.…”

Section: Enzymes Of Phospholipid Synthesismentioning

confidence: 99%

Lung surfactant.

Rooney¹

1984

Environ Health Perspect

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Aspects of pulmonary surfactant are reviewed from a biochemical perspective. The major emphasis is on the lipid components of surfactant. Topics reviewed include surfactant composition, cellular and subcellular sites as well as pathways of biosynthesis of phosphatidylcholine, disaturated phosphatidylcholine and phosphatidylglycerol. The surfactant system in the developing fetus and neonate is considered in terms of phospholipid content and composition, rates of precursor incorporation, activities of individual enzymes of phospholipid synthesis and glycogen content and metabolism. The influence of the following hormones and other factors on lung maturation and surfactant production is discussed: glucocorticoids, thyroid hormone, estrogen, prolactin, cyclic AMP, p-adrenergic and cholinergic agonists, prostaglandins and growth factors. The influence of maternal diabetes, fetal sex, stress and labor are also considered. Nonphysiologic and toxic agents which influence surfactant in the fetus, newborn and adult are reviewed.

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“…Surfactant complex from normal adults contains, other than lecithins (-70% of total lecithin is disaturated, containing predominantly palmitate), phosphatidylglycerol in uniquely high concentration, phosphatidylethanolamine, phosphatidylinositol, cholesterol, small amounts of some other lipids, and, at the least one surfactant-specific protein that seems to possess phosphatidate phosphohydrolase activity (16)(17)(18)(19). However, during fetal development, before the final maturation of the surfactant system, the complex contains no phosphatidylglycerol, but instead very high levels of phosphatidylinositol (15,19).…”

mentioning

confidence: 99%

Evidence of lung surfactant abnormality in respiratory failure. Study of bronchoalveolar lavage phospholipids, surface activity, phospholipase activity, and plasma myoinositol.

Hallman¹,

Spragg²,

Harrell³

et al. 1982

J. Clin. Invest.

428

144

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A B S T R A C T Autopsy findings suggest that lung surfactant is damaged in the adult respiratory distress syndrome. In the present study 225 bronchoalveolar lavage specimens (78 from 36 patients, 1-78 yr old with respiratory failure, 135 from another 128 patients with other respiratory disease, and 12 from healthy controls) were assayed for the lung profile [lecithin/ sphingomyelin (L/S) ratio, saturated lecithin, phosphatidylinositol, and phosphatidylglycerol]. Bronchoalveolar lavage fluid was further analyzed for phospholipids and for phosphatidic acid phosphohydrolase, phospholipase A2, and phosphatidylinositol phosphodiesterase activities. A lipid-protein complex was isolated and analyzed for surface activity, and plasma was measured for myoinositol.There were only small differences seen in the recovery of total phospholipid between respiratory failure patients and normal controls. However, in respiratory failure, phospholipids in bronchoalveolar lavage were qualitatively different from those recovered either from normal controls or from patients with other lung disease: the L/S ratio, phosphatidylglycerol, and disaturated lecithin were low, whereas sphingomyelin and phosphatidylserine were prominent. These abnormalities were present early in respiratory failure A preliminary report of this work was presented at the

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Properties of an acid phosphatase in pulmonary surfactant.

Cited by 16 publications

References 29 publications

Modifications of Pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells

Modifications of Pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells

Lung surfactant.

Evidence of lung surfactant abnormality in respiratory failure. Study of bronchoalveolar lavage phospholipids, surface activity, phospholipase activity, and plasma myoinositol.

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