Innate immune response triggered by triacyl lipid A is dependent on phospholipid transfer protein (PLTP) gene expression.
Fiche publication
Date publication
septembre 2010
Auteurs
Membres identifiés du Cancéropôle Est :
Pr BETTAIEB Ali
Tous les auteurs :
Gautier T, Paul C, Deckert V, Desrumaux C, Klein A, Labbe J, Le Guern N, Athias A, Monier S, Hammann A, Bettaieb A, Jeannin JF, Lagrost L
Lien Pubmed
Résumé
Hexaacyl lipopolysaccharide (LPS) aggregates in aqueous media, but its partially deacylated lipid A moiety forms monomers with weaker toxicity. Because plasma phospholipid transfer protein (PLTP) transfers hexaacyl LPS, its impact on metabolism and biological activity of triacyl lipid A in mice was addressed. Triacyl lipid A bound readily to plasma high-density lipoproteins (HDLs) when active PLTP was expressed [HDL-associated lipid A after 4.5 h: 59.1+/-16.0% of total in wild-type (WT) vs. 32.5+/-10.3% in PLTP-deficient mice, P
Référence
FASEB J. 2010 Sep;24(9):3544-54