ApoE-containing high density lipoproteins and phospholipid transfer protein activity increase in patients with a systemic inflammatory response

Barlage, Stefan; Fröhlich, D.; Böttcher, Alfred; Jauhiainen, Matti; Müller, Hans Peter; Noetzel, Felicitas; Rothe, Gregor; Schütt, Christine; Linke, Reinhold P.; Lackner, Karl J.; Ehnholm, Christian; Schmitz, Gerd

doi:10.1016/s0022-2275(20)31690-4

Cited by 107 publications

(21 citation statements)

References 38 publications

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“…Irrespective of the source of the cholesterol, the liver repacks the excess cholesterol into VLDL-c and releases them into the bloodstream. Endothelial lipoprotein lipase (LPL) catalyses triglyceride and facilitates receptor-mediated cholesterol uptake, relying on ApoE and ApoB100 [ 123 , 124 ]. This allows endothelium to be supplied with triglycerides and, to a very limited degree, with cholesterol.…”

Section: Lipid Metabolism Under Nominal Conditionsmentioning

confidence: 99%

“…A modification accompanied the HDL-c composition decreased with increased serum amyloid A concentration during recovery [ 136 ]. This alteration in HDL-c composition is linked to increased platelet levels and monocyte activation, potentially accelerating atherosclerosis [ 123 , 139 ]. Amyloid A may be implicated in the exacerbation of diastolic heart dysfunction.…”

Section: Lipid Metabolism During In Sepsis Survivorsmentioning

confidence: 99%

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Persistence of Lipoproteins and Cholesterol Alterations after Sepsis: Implication for Atherosclerosis Progression

Laudański

2021

IJMS

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(1) Background: Sepsis is one of the most common critical care illnesses with increasing survivorship. The quality of life in sepsis survivors is adversely affected by several co-morbidities, including increased incidence of dementia, stroke, cardiac disease and at least temporary deterioration in cognitive dysfunction. One of the potential explanations for their progression is the persistence of lipid profile abnormalities induced during acute sepsis into recovery, resulting in acceleration of atherosclerosis. (2) Methods: This is a targeted review of the abnormalities in the long-term lipid profile abnormalities after sepsis; (3) Results: There is a well-established body of evidence demonstrating acute alteration in lipid profile (HDL-c ↓↓, LDL-C -c ↓↓). In contrast, a limited number of studies demonstrated depression of HDL-c levels with a concomitant increase in LDL-C -c in the wake of sepsis. VLDL-C -c and Lp(a) remained unaltered in few studies as well. Apolipoprotein A1 was altered in survivors suggesting abnormalities in lipoprotein metabolism concomitant to overall lipoprotein abnormalities. However, most of the studies were limited to a four-month follow-up and patient groups were relatively small. Only one study looked at the atherosclerosis progression in sepsis survivors using clinical correlates, demonstrating an acceleration of plaque formation in the aorta, and a large metanalysis suggested an increase in the risk of stroke or acute coronary event between 3% to 9% in sepsis survivors. (4) Conclusions: The limited evidence suggests an emergence and persistence of the proatherogenic lipid profile in sepsis survivors that potentially contributes, along with other factors, to the clinical sequel of atherosclerosis.

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Section: Lipid Metabolism Under Nominal Conditionsmentioning

confidence: 99%

Section: Lipid Metabolism During In Sepsis Survivorsmentioning

confidence: 99%

Persistence of Lipoproteins and Cholesterol Alterations after Sepsis: Implication for Atherosclerosis Progression

Laudański

2021

IJMS

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“…It also agrees with in vitro and in vivo studies in preclinical models [including PLTP-knocked out mice and the infusion of active recombinant human PLTP in mice with experimental sepsis (15,19,22,27)] which have revealed that the PLTP-mediated transfer of LPS to lipoproteins results in neutralization of the pro-inflammatory properties of LPS and in its elimination from the body. Elevated PLTP activity was also reported in patients with severe sepsis (28,29) and during the acute-phase response induced by infection (26). Taken together, the previous reports and the present results strongly suggest that PLTP activity may adapt to and eliminate the culprit endotoxins in patients with septic shock.…”

Section: Discussionsupporting

confidence: 86%

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“…Similar to what reported in mice, subjects with low plasma HDL levels (hypoalphalipoproteinemia) present an increased prevalence of classical CD14++/CD16À but not of intermediate CD14++/CD16+ monocytes, further linking HDL-to LPS-mediated responses . Septic HDLs are almost depleted of apoC-I ( Barlage et al 2001). ApoC-I contains a consensus LPS-binding motif and is able to enhance the biological response to LPS thus reducing mortality in mice with Gram-negative-induced sepsis (Berbee et al 2006).…”

Section: Interaction Of Hdl With Lps and Gram-negative Bacteriamentioning

confidence: 99%

High Density Lipoproteins

Rj²,

Jw³

2015

Handbook of Experimental Pharmacology

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ApoE-containing high density lipoproteins and phospholipid transfer protein activity increase in patients with a systemic inflammatory response

Cited by 107 publications

References 38 publications

Persistence of Lipoproteins and Cholesterol Alterations after Sepsis: Implication for Atherosclerosis Progression

Persistence of Lipoproteins and Cholesterol Alterations after Sepsis: Implication for Atherosclerosis Progression

Table_1.DOCX

High Density Lipoproteins

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