Sphingomyelin and phosphatidylcholine contrarily affect the induction of apoptosis in intestinal epithelial cells
Version of Record online: 20 OCT 2013
© 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
Molecular Nutrition & Food Research
Volume 58, Issue 4, pages 782–798, April 2014
How to Cite
Leucht, K., Fischbeck, A., Caj, M., Liebisch, G., Hartlieb, E., Benes, P., Fried, M., Humpf, H.-U., Rogler, G. and Hausmann, M. (2014), Sphingomyelin and phosphatidylcholine contrarily affect the induction of apoptosis in intestinal epithelial cells. Mol. Nutr. Food Res., 58: 782–798. doi: 10.1002/mnfr.201300369
- Issue online: 1 APR 2014
- Version of Record online: 20 OCT 2013
- Manuscript Accepted: 20 AUG 2013
- Manuscript Revised: 14 AUG 2013
- Manuscript Received: 22 MAY 2013
- Swiss National Science Foundation. Grant Numbers: SNF 31003A_127247 to MH, SNF 310030 120312 to GR
- Agency of Ministry of Health of the Czech Republic. Grant Number: NT 13441-4/2012
- European Regional Development Fund
- Project FNUSA-ICRC. Grant Number: CZ.1.05/1.1.00/02.0123
- Cathepsin D;
The major alimentary sources for the plasma membrane lipid sphingomyelin (SM) are dairy products, eggs, and meat. We recently reported that the SM metabolite ceramide induces cathepsin D mediated apoptosis in murine intestinal epithelial cells (IECs) and increases inflammation in acute colitis. We investigated the impact of SM and phosphatidylcholine on apoptosis in human IECs and point out BH3-interacting death agonist (BID) as link between cathepsin D and apoptosis.
Methods and results
HT-29 and isolated human IECs were stimulated with SM or phosphatidylcholine. SM treatment resulted in increased apoptosis. Phosphatidylcholine showed contrary effects. Western revealed higher amounts of cathepsin D and BID activation upon lipid stimulation. Western blotting revealed BID activation through SM in both an induced and a spontaneous mouse model of colitis.
Dietary phospholipids may induce or abolish apoptosis in IECs and seem to play a role in the pathogenesis of inflammatory bowel diseases. This nutritional factor might be considered when evaluating the pathogenesis of inflammatory bowel diseases. Effects of SMase- and SM treatment on inflammation in dextran sulfate sodium induced animal models of colitis and in vitro experiments are discussed as controversial. Variable sources of SM, feeding techniques, and mouse strains might play a role.