Hydrolysis of Surfactant Phospholipids Catalyzed by Phospholipase A2 and Eosinophil Lysophospholipases Causes Surfactant Dysfunction

Ackerman, Steven J.; Kwatia, Mark A.; Doyle, Christine B.; Enhörning, Göran

doi:10.1378/chest.123.3_suppl.355s

Cited by 35 publications

(29 citation statements)

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“…During asthma exacerbations infl ammatory cells release phospholipase A2 into the airway, which hydrolyzes phosphatidylcholine, the principal component of surfactant. [9] Thus, the low level of serum carnitine in our asthmatic children during or shortly after (3 weeks in this study) asthmatic attack might be attributed to decreased lung surfactant (during attack) and the use of body stores to replenish it (after attack). Moreover, serum free carnitine levels were reported to be decreased in children with recurrent pulmonary infections.…”

Section: Discussionmentioning

confidence: 67%

Serum total and free carnitine levels in children with asthma

et al. 2009

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Section: Discussionmentioning

confidence: 67%

Serum total and free carnitine levels in children with asthma

et al. 2009

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“…However, synthetic ether-linked lipids are now available that have direct structural analogy to lung surfactant lipids plus designed molecular behavior that enhances adsorption and spreading while maintaining very high dynamic surface tension lowering in surface films (e.g., [71,[205][206][207][208][209][210][211]). Moreover, such lipids have structural features making them resistant to phospholipases such as phospholipase A 2 , which has been implicated in the pathology of ALI/ARDS [65,[212][213][214][215][216][217][218]. Phospholipase-induced degradation of lung surfactant glycerophospholipids not only reduces the concentration of active components, but also generates reaction products such as lysophosphatidylcholine and fluid free fatty acids that can further decrease surface activity by interacting biophysically with remaining surfactant at the alveolar interface [55,59,70].…”

Section: Examples Of Research On New Synthetic Exogenous Surfactamentioning

confidence: 99%

Surfactant for Pediatric Acute Lung Injury

Willson¹,

Chess²,

Notter³

2008

Pediatric Clinics of North America

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SynopsisThis article reviews exogenous surfactant therapy and its use in mitigating acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS) in infants, children, and adults. Biophysical and animal research documenting surfactant dysfunction in ALI/ARDS is described, and the scientific rationale for treatment with exogenous surfactant is discussed. Major emphasis is on reviewing clinical studies of surfactant therapy in pediatric and adult patients with ALI/ARDS. Particular advantages from surfactant therapy in direct pulmonary forms of these syndromes are described. Also discussed are additional factors affecting the efficacy of exogenous surfactants in ALI/ARDS, including the multifaceted pathology of inflammatory lung injury, the effectiveness of surfactant delivery in injured lungs, and composition-based activity differences among clinical exogenous surfactant preparations.

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“…In addition to animal-derived surfactants such as Infasurf, highly-active new synthetic lipid/peptide lung surfactants are currently being developed that have significant potential advantages in manufacturing, economy, and purity compared to biological products [202][203][204][205][206][207]. Such synthetic surfactants include preparations with novel physicochemical properties like phospholipase-resistance [203][204][205][206][207], which may be of particular importance in ALI/ARDS where these lytic enzymes can be elaborated in high concentrations in the interstitium and alveoli [208][209][210][211][212][213][214].…”

Section: Exogenous Surfactant Therapy For Acute Phase Ali/ardsmentioning

confidence: 99%

Pharmacotherapy of Acute Lung Injury and Acute Respiratory Distress Syndrome

Raghavendran¹,

Pryhuber²,

Chess³

et al. 2008

CMC

111

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Acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS) are characterized by rapid-onset respiratory failure following a variety of direct and indirect insults to the parenchyma or vasculature of the lungs. Mortality from ALI/ARDS is substantial, and current therapy primarily emphasizes mechanical ventilation and judicial fluid management plus standard treatment of the initiating insult and any known underlying disease. Current pharmacotherapy for ALI/ARDS is not optimal, and there is a significant need for more effective medicinal chemical agents for use in these severe and lethal lung injury syndromes. To facilitate future chemical-based drug discovery research on new agent development, this paper reviews present pharmacotherapy for ALI/ARDS in the context of biological and biochemical drug activities. The complex lung injury pathophysiology of ALI/ ARDS offers an array of possible targets for drug therapy, including inflammation, cell and tissue injury, vascular dysfunction, surfactant dysfunction, and oxidant injury. Added targets for pharmacotherapy outside the lungs may also be present, since multiorgan or systemic pathology is common in ALI/ARDS. The biological and physiological complexity of ALI/ARDS requires the consideration of combined-agent treatments in addition to single-agent therapies. A number of pharmacologic agents have been studied individually in ALI/ARDS, with limited or minimal success in improving survival. However, many of these agents have complementary biological/biochemical activities with the potential for synergy or additivity in combination therapy as discussed in this article.

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Hydrolysis of Surfactant Phospholipids Catalyzed by Phospholipase A2 and Eosinophil Lysophospholipases Causes Surfactant Dysfunction

Cited by 35 publications

References 0 publications

Serum total and free carnitine levels in children with asthma

Serum total and free carnitine levels in children with asthma

Surfactant for Pediatric Acute Lung Injury

Pharmacotherapy of Acute Lung Injury and Acute Respiratory Distress Syndrome

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