Bacterial infection triggers an acute inflammatory response that might alter phospholipid metabolism. We have investigated the acute-phase response of murine lung epithelia to Pseudomonas aeruginosa infection. Ps. aeruginosa triggered secretion of the pro-inflammatory lipase, sPLA2 IB (phospholipase A2 IB), from lung epithelium. Ps. aeruginosa and sPLA2 IB each stimulated basolateral PtdCho (phosphatidylcholine) efflux in lung epithelial cells. Pre-treatment of cells with glyburide, an inhibitor of the lipid-export pump, ABCA1 (ATP-binding cassette transporter A1), attenuated Ps. aeruginosa and sPLA2 IB stimulation of PtdCho efflux. Effects of Ps. aeruginosa and sPLA2 IB were completely abolished in human Tangier disease fibroblasts, cells that harbour an ABCA1 genetic defect. Ps. aeruginosa and sPLA2 IB induced the heterodimeric receptors, PPARα (peroxisome-proliferator-activated receptor-α) and RXR (retinoid X receptor), factors known to modulate ABCA1 gene expression. Ps. aeruginosa and sPLA2 IB stimulation of PtdCho efflux was blocked with PD98059, a p44/42 kinase inhibitor. Transfection with MEK1 (mitogen-activated protein kinase/extracellular-signal-regulated kinase kinase 1), a kinase upstream of p44/42, increased PPARα and RXR expression co-ordinately with increased ABCA1 protein. These results suggest that pro-inflammatory effects of Ps. aeruginosa involve release of an sPLA2 of epithelial origin that, in part, via distinct signalling molecules, transactivates the ABCA1 gene, leading to export of phospholipid.
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Research Article|
April 12 2007
Pseudomonas aeruginosa and sPLA2 IB stimulate ABCA1-mediated phospholipid efflux via ERK-activation of PPARα–RXR
Marianna Agassandian;
Marianna Agassandian
1
*Department of Internal Medicine, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, U.S.A.
1To whom correspondence should be addressed (email [email protected]).
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Olga L. Miakotina;
Olga L. Miakotina
*Department of Internal Medicine, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, U.S.A.
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Matthew Andrews;
Matthew Andrews
*Department of Internal Medicine, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, U.S.A.
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Satya N. Mathur;
Satya N. Mathur
*Department of Internal Medicine, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, U.S.A.
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Rama K. Mallampalli
Rama K. Mallampalli
*Department of Internal Medicine, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, U.S.A.
†Department of Biochemistry, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, U.S.A.
‡Department of Veterans Affairs Medical Center, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, U.S.A.
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Publisher: Portland Press Ltd
Received:
September 05 2006
Revision Received:
January 02 2007
Accepted:
January 16 2007
Accepted Manuscript online:
January 16 2007
Online ISSN: 1470-8728
Print ISSN: 0264-6021
The Biochemical Society, London
2007
Biochem J (2007) 403 (3): 409–420.
Article history
Received:
September 05 2006
Revision Received:
January 02 2007
Accepted:
January 16 2007
Accepted Manuscript online:
January 16 2007
Citation
Marianna Agassandian, Olga L. Miakotina, Matthew Andrews, Satya N. Mathur, Rama K. Mallampalli; Pseudomonas aeruginosa and sPLA2 IB stimulate ABCA1-mediated phospholipid efflux via ERK-activation of PPARα–RXR. Biochem J 1 May 2007; 403 (3): 409–420. doi: https://doi.org/10.1042/BJ20061364
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