title: Sphingomyelin and phosphatidylcholine contrarily affect the induction of apoptosis in intestinal epithelial cells.
abstract: METHODS
  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.
  
  
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Internal Medicine, Division of Gastroenterology and Hepatology, University Hospital Zurich, Switzerland.
authors.forename: Katharina
authors.initials: K
authors.lastname: Leucht
authors.forename: Anne
authors.initials: A
authors.lastname: Fischbeck
authors.forename: Michaela
authors.initials: M
authors.lastname: Caj
authors.forename: Gerhard
authors.initials: G
authors.lastname: Liebisch
authors.forename: Eva
authors.initials: E
authors.lastname: Hartlieb
authors.forename: Petr
authors.initials: P
authors.lastname: Benes
authors.forename: Michael
authors.initials: M
authors.lastname: Fried
authors.forename: Hans-Ulrich
authors.initials: HU
authors.lastname: Humpf
authors.forename: Gerhard
authors.initials: G
authors.lastname: Rogler
authors.forename: Martin
authors.initials: M
authors.lastname: Hausmann
mesh_terms: D022005:Adherens Junctions / Q000187:drug effects; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D051023:BH3 Interacting Domain Death Agonist Protein / Q000378:metabolism; D002402:Cathepsin D / Q000378:metabolism; D016923:Cell Death / Q000187:drug effects; D002478:Cells, Cultured; D002518:Ceramides / Q000378:metabolism; D003092:Colitis / Q000378:metabolism / Q000473:pathology; D019587:Dietary Supplements; D004847:Epithelial Cells / Q000187:drug effects* / Q000473:pathology; D005260:Female; D019073:HT29 Cells / Q000187:drug effects; D006801:Humans; D007422:Intestines / Q000166:cytology*; D008081:Liposomes / Q000494:pharmacology; D008810:Mice, Inbred C57BL; D010713:Phosphatidylcholines / Q000378:metabolism / Q000494:pharmacology*; D013108:Sphingomyelin Phosphodiesterase / Q000378:metabolism; D013109:Sphingomyelins / Q000378:metabolism / Q000494:pharmacology*
chemical_list: D051023:BH3 Interacting Domain Death Agonist Protein; C494814:BID protein, human; D002518:Ceramides; D008081:Liposomes; D010713:Phosphatidylcholines; D013109:Sphingomyelins; D013108:Sphingomyelin Phosphodiesterase; C533922:CTSD protein, human; D002402:Cathepsin D
keywords: Apoptosis; BID; Cathepsin D; Phosphatidylcholine; Sphingomyelin