Bioactive Lysophosphatidylcholine 16:0 and 18:0 Are Elevated in Lungs of Asthmatic Subjects.
- Author:
Mark YODER
1
;
Yan ZHUGE
;
Yang YUAN
;
Oksana HOLIAN
;
Sherry KUO
;
Richard VAN BREEMEN
;
Larry L THOMAS
;
Hazel LUM
Author Information
- Publication Type:Original Article
- Keywords: Lysophosphatidylcholine; asthma; phospholipase A2
- MeSH: Asthma; Cardiovascular Diseases; Fatty Acids, Nonesterified; Lung*; Lysophosphatidylcholines*; Mass Spectrometry; Phosphatidylcholines; Phospholipases A2; Therapeutic Irrigation; Up-Regulation
- From:Allergy, Asthma & Immunology Research 2014;6(1):61-65
- CountryRepublic of Korea
- Language:English
- Abstract: PURPOSE: Asthma is a chronic inflammatory disease of the airways, and is associated with upregulation of phospholipase A2 (PLA2), the enzyme that hydrolyzes phosphatidylcholine, producing lysophosphatidylcholine (LPC) and free fatty acids. LPC is a lipid mediator with known pro-inflammatory and pro-atherogenic properties, and is believed to be a critical factor in cardiovascular diseases. We postulate that asthmatic subjects have an elevated content of LPC in the lung lining fluids. METHODS: Eight non-asthmatic controls and seven asthmatic subjects were recruited for broncho-alveolar lavage fluids (BALF) collection for analysis of LPC by high performance liquid chromatography-tandem mass spectrometry. RESULTS: LPC16:0 and LPC18:0 were significantly elevated in the BALF of asthmatics with impaired lung function characteristic of moderate asthma, but not mild asthma. The increased LPC content in BALF was accompanied by increased PLA2 activity. Furthermore, qRT-PCR analysis of the BALF cell fraction indicated increased secretory PLA2-X (sPLA2-X). CONCLUSIONS: The increased LPC content in the lung lining fluids is a potential critical lipid mediator in the initiation and/or progression of airway epithelial injury in asthma.
