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In Vivo Inflammation Does Not Impair ABCA1-Mediated Cholesterol Efflux Capacity of HDL

HDL provides atheroprotection by facilitating cholesterol efflex from lipid-laden macrophages in the vessel wall. In vitro studies have suggested impaired efflux capacity of HDL following inflammatory changes. We assessed the impact of acute severe sepsis and mild chronic inflammatory disease on the... Full description

Journal Title: Cholesterol 2012-12-01, Vol.2012, p.610741-8
Main Author: Franssen, Remco
Other Authors: Schimmel, Alinda W. M , van Leuven, Sander I , Wolfkamp, Simone C. S , Stroes, Erik S. G , Dallinga-Thie, Geesje M
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: United States: Hindawi Limiteds
ID: ISSN: 2090-1283
Link: https://www.ncbi.nlm.nih.gov/pubmed/22611487
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recordid: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3348631
title: In Vivo Inflammation Does Not Impair ABCA1-Mediated Cholesterol Efflux Capacity of HDL
format: Article
creator:
  • Franssen, Remco
  • Schimmel, Alinda W. M
  • van Leuven, Sander I
  • Wolfkamp, Simone C. S
  • Stroes, Erik S. G
  • Dallinga-Thie, Geesje M
subjects:
  • Article Subject
  • Cardiovascular disease
  • Cholesterol
  • Diseases of the circulatory (Cardiovascular) system
  • lipids (amino acids
  • metabolic diseases
  • Mortality
  • nutritional
  • peptides
  • Proteins
  • Research Article
ispartof: Cholesterol, 2012-12-01, Vol.2012, p.610741-8
description: HDL provides atheroprotection by facilitating cholesterol efflex from lipid-laden macrophages in the vessel wall. In vitro studies have suggested impaired efflux capacity of HDL following inflammatory changes. We assessed the impact of acute severe sepsis and mild chronic inflammatory disease on the efflux capacity of HDL. We hypothesize that a more severe inflammatory state leads to stronger impaired cholesterol efflux capacity. Using lipid-laden THP1 cells and fibroblasts we were able to show that efflux capacity of HDL from both patients with severe sepsis or with Crohn's disease (active or in remission), either isolated using density gradient ultracentrifugation or using apoB precipitation, was not impaired. Yet plasma levels of HDL cholesterol and apoA-I were markedly lower in patients with sepsis. Based on the current observations we conclude that inflammatory disease does not interfere with the capacity of HDL to mediate cholesterol efflux. Our findings do not lend support to the biological relevance of HDL function changes in vitro.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 2090-1283
fulltext: fulltext
issn:
  • 2090-1283
  • 2090-1291
  • 2090-1291
url: Link


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descriptionHDL provides atheroprotection by facilitating cholesterol efflex from lipid-laden macrophages in the vessel wall. In vitro studies have suggested impaired efflux capacity of HDL following inflammatory changes. We assessed the impact of acute severe sepsis and mild chronic inflammatory disease on the efflux capacity of HDL. We hypothesize that a more severe inflammatory state leads to stronger impaired cholesterol efflux capacity. Using lipid-laden THP1 cells and fibroblasts we were able to show that efflux capacity of HDL from both patients with severe sepsis or with Crohn's disease (active or in remission), either isolated using density gradient ultracentrifugation or using apoB precipitation, was not impaired. Yet plasma levels of HDL cholesterol and apoA-I were markedly lower in patients with sepsis. Based on the current observations we conclude that inflammatory disease does not interfere with the capacity of HDL to mediate cholesterol efflux. Our findings do not lend support to the biological relevance of HDL function changes in vitro.
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subjectArticle Subject ; Cardiovascular disease ; Cholesterol ; Diseases of the circulatory (Cardiovascular) system ; lipids (amino acids ; metabolic diseases ; Mortality ; nutritional ; peptides ; Proteins ; Research Article
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abstractHDL provides atheroprotection by facilitating cholesterol efflex from lipid-laden macrophages in the vessel wall. In vitro studies have suggested impaired efflux capacity of HDL following inflammatory changes. We assessed the impact of acute severe sepsis and mild chronic inflammatory disease on the efflux capacity of HDL. We hypothesize that a more severe inflammatory state leads to stronger impaired cholesterol efflux capacity. Using lipid-laden THP1 cells and fibroblasts we were able to show that efflux capacity of HDL from both patients with severe sepsis or with Crohn's disease (active or in remission), either isolated using density gradient ultracentrifugation or using apoB precipitation, was not impaired. Yet plasma levels of HDL cholesterol and apoA-I were markedly lower in patients with sepsis. Based on the current observations we conclude that inflammatory disease does not interfere with the capacity of HDL to mediate cholesterol efflux. Our findings do not lend support to the biological relevance of HDL function changes in vitro.
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