title: ApoE-containing high density lipoproteins and phospholipid transfer protein activity increase in patients with a systemic inflammatory response.
abstract: High density lipoproteins (HDL) mediate reverse cholesterol transport as well as the clearance of oxidation products or inflammatory mediators, thereby contributing to tissue integrity. The decrease in HDL in inflammation has been attributed to decreased lecithin:cholesterol acyltransferase activity, whereas the role of phospholipid transfer protein (PLTP) and cholesteryl ester transfer protein has not been analyzed in detail. We have studied the activities of HDL-modifying proteins and the heterogeneity of HDL in healthy control subjects and three groups of postsurgery patients: no bacterial infection (group 1), bacterial focus and systemic inflammatory response (group 2), and severe sepsis (group 3). For all patients, a decrease in total HDL could be demonstrated, with a loss of mainly large, apolipoprotein A-I (apoA-I) HDL particles, an almost total loss of apoC-I, and an increase in apoE HDL (200-500 kDa), which did not contain significant amounts of apoA-I, apoA-II, or apoC-I. PLTP activity was increased in patients of groups 2 and 3, paralleled by a redistribution of PLTP into a population of small (120- to 200-kDa) particles, probably representing PLTP homodimers or lipid-complexed PLTP. In summary, the increase in apoE HDL and PLTP activity may improve the delivery of energy substrates and phospholipids to tissues that must maintain cellular membrane homeostasis under conditions of inflammatory stress.
authors.affiliation: Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, D-93042 Regensburg, Germany.
authors.forename: S
authors.initials: S
authors.lastname: Barlage
authors.forename: D
authors.initials: D
authors.lastname: Fröhlich
authors.forename: A
authors.initials: A
authors.lastname: Böttcher
authors.forename: M
authors.initials: M
authors.lastname: Jauhiainen
authors.forename: H P
authors.initials: HP
authors.lastname: Müller
authors.forename: F
authors.initials: F
authors.lastname: Noetzel
authors.forename: G
authors.initials: G
authors.lastname: Rothe
authors.forename: C
authors.initials: C
authors.lastname: Schütt
authors.forename: R P
authors.initials: RP
authors.lastname: Linke
authors.forename: K J
authors.initials: KJ
authors.lastname: Lackner
authors.forename: C
authors.initials: C
authors.lastname: Ehnholm
authors.forename: G
authors.initials: G
authors.lastname: Schmitz
mesh_terms: D000328:Adult; D000368:Aged; D001057:Apolipoproteins E / Q000097:blood / Q000378:metabolism*; D002352:Carrier Proteins / Q000097:blood / Q000378:metabolism*; D015180:Electrophoresis, Gel, Two-Dimensional; D005260:Female; D006801:Humans; D008055:Lipids / Q000097:blood; D008075:Lipoproteins, HDL / Q000097:blood / Q000737:chemistry / Q000302:isolation & purification / Q000378:metabolism*; D008297:Male; D008565:Membrane Proteins / Q000097:blood / Q000378:metabolism*; D008875:Middle Aged; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000378:metabolism; D049294:Phospholipid Transfer Proteins; D018805:Sepsis / Q000378:metabolism*
chemical_list: D001057:Apolipoproteins E; D002352:Carrier Proteins; D008055:Lipids; D008075:Lipoproteins, HDL; D008565:Membrane Proteins; D049294:Phospholipid Transfer Proteins; D007862:Phosphatidylcholine-Sterol O-Acyltransferase