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Allergy Asthma Immunol Res. 2014 Jan;6(1):61-5. doi: 10.4168/aair.2014.6.1.61. Epub 2013 Dec 5.

Bioactive lysophosphatidylcholine 16:0 and 18:0 are elevated in lungs of asthmatic subjects.

Author information

1
Department of Medicine, Rush University Medical Center, Chicago, IL, USA.
2
Department of Pharmacology, Rush University Medical Center, Chicago, IL, USA.
3
Department of Medicinal Chemistry & Pharmacognosy, University of Illinois, Chicago, IL, USA.
4
Department of Immunology and Microbiology, Rush University Medical Center, Chicago, IL, USA.

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.

KEYWORDS:

Lysophosphatidylcholine; asthma; phospholipase A2

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