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• W2097638868 abstract "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<0.05]. In the opposite to hexaacyl LPS, plasma residence time of lipid A was extended by PLTP, and proinflammatory cytokines were produced in higher amounts in WT than PLTP−/− mice (remaining lipid A after 8 h: 53±12 vs. 35±7%, and IL6 concentration after 4.5 h: 45.5±5.9 vs. 14.6±7.8 ng/ml, respectively;P<0.05 in all cases). After 1 wk, onset of B16-induced melanoma was observed in only 30% of lipid A-treated WT mice, whereas >80% of the untreated WT, untreated PLTP-deficient, or lipid A-treated PLTP-deficient animals bore tumors (P<0.05 in all cases). It is concluded that PLTP is essential in mediating the association of triacyl lipid A with lipoproteins, leading to extension of its residence time and to magnification of its proinflammatory and anticancer properties.—Gautier, T., Paul, C., Deckert, v., Desrumaux, C., Klein, A., Labbe, J., Le Guern, N., Athias, A., Monier, S., Hammann, A., Bettaieb, A., Jeannin, J.-F., Lagrost, L. Innate immune response triggered by triacyl lipid A is dependent on phospholipid transfer protein (PLTP) gene expression. FASEB J. 24, 3544–3554 (2010). www.fasebj.org" @default.
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• W2097638868 date "2010-04-23" @default.
• W2097638868 modified "2023-10-18" @default.
• W2097638868 title "Innate immune response triggered by triacyl lipid A is dependent on phospholipid transfer protein (PLTP) gene expression" @default.
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• W2097638868 doi "https://doi.org/10.1096/fj.09-152876" @default.
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