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Hydrolysis of Surfactant Phospholipids Catalyzed by Phospholipase A2 and Eosinophil Lysophospholipases Causes Surfactant Dysfunction*: A Mechanism for Small Airway Closure in Asthma

Steven J. Ackerman, PhD; Mark A. Kwatia, MS; Christine B. Doyle, BA; Goran Enhorning, MD
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*From the University of Illinois at Chicago (Dr. Ackerman, Mr. Kwatia and Ms. Doyle), Chicago, IL; and the State University of New York at Buffalo (Dr. Enhorning), Buffalo, NY.

Correspondence to: Steven J. Ackerman, PhD, Department of Biochemistry and Molecular Biology (MC536), A-312 College of Medicine West, 1819 West Polk St, Chicago, IL 60612-7334; e-mail: sackerma@uic.edu



Chest. 2003;123(3_suppl):355S. doi:10.1378/chest.123.3_suppl.355S
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During asthma exacerbations, there is increased release of phospholipase A2 (PLA2) from inflammatory cells into the airway. PLA2 has the capacity to hydrolyze the principal component of pulmonary surfactant, phosphatidylcholine (PC), which is responsible for maintaining airway patency in terminal bronchioles and alveoli. The products of PLA2 hydrolysis of PC include fatty acids such as palmitic acid (PA) and lysophosphatidylcholine (LPC). The LPC then may serve as a substrate for eosinophil lysophospholipases (LPLases). LPLases are expressed by eosinophils in the lung in murine models of asthma, and surfactant dysfunction recently has been identified in patients with asthma exacerbations, as well as allergic subjects undergoing experimental segmental lung allergen challenges.

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