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Phospholipid cellular uptake mediated by cationic lipids affects the inflammatory response
Author(s) -
Lonez Caroline,
Vandenbranden Michel,
Legat Amandine,
Ruysschaert JeanMarie
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1037.3
Subject(s) - cationic polymerization , liposome , cationic liposome , phospholipid , chemistry , secretion , biochemistry , inflammation , biology , transfection , immunology , membrane , organic chemistry , gene
We show here that free cationic liposomes inhibit CpG sequences or lipopolysaccharides‐induced TNF‐α secretion by macrophages. Surprisingly, this effect was strictly serum‐dependent. Free cationic liposomes alone did not reveal any anti‐inflammatory activity. By serum fractionation on a density gradient, low‐density lipoproteins and triglyceride‐rich lipoproteins were identified as the serum components that confer to the liposomes an anti‐inflammatory activity1. Phospholipid fractions of these lipoproteins reproduced the effect of the total lipoproteins and could inhibit, in association with diC14‐amidine, the CpG‐induced TNF‐α secretion. Whereas oxidation of LDL phospholipids was a prerequisite to any anti‐inflammatory activity, lipid oxidation is no more required when phospholipids are transported in cationic liposomes. This suggests that cationic mediated‐transport of phospholipids (PC, PS, PE, PG) proceeds through a different route and affects different pathways. Cationic liposomes confer to these phospholipids new properties that can be used to modulate the inflammatory response directed against CpG sequences and lipopolysaccharides.