Evidence map›Paper›PMID 11292694›Full record

ArticleInfection and immunity2001

Distribution and kinetics of lipoprotein-bound endotoxin.

J H Levels, P R Abraham, A van den Ende, S J van Deventer

Registry-linked trialAbstract read
In one paragraph

Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03869073 (Randomized, Double-blind, Placebo-controlled Phase 2a Trial of Efficacy and Safety of Evolocumab for PCSK9 Lowering in Early Acute Sepsis), which is not on this map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
2.1field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT03869073 phase2unknown statusnot on this mapstarted 2019, after this paper: background citation

Randomized, Double-blind, Placebo-controlled Phase 2a Trial of Efficacy and Safety of Evolocumab for PCSK9 Lowering in Early Acute Sepsis

TypeinterventionalSponsorUniversity of British ColumbiaRan2019 to 2021Enrolled36ConditionsSepsisArmsEvolocumab, Placebo
3 · Its place in the literature

Who cites it

85 citing papers in PubMed, 233 citations in OpenAlex.

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25 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

J H LevelsDepartment of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands. h.levels@amc.uva.nl
P R Abraham
A van den Ende
S J van Deventer
Academic Medical Center · NLCenter for Vascular Biology Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipopolysaccharide (LPS), the major glycolipid component of gram-negative bacterial outer membranes, is a potent endotoxin responsible for pathophysiological symptoms characteristic of infection. The observation that the majority of LPS is found in association with plasma lipoproteins has prompted the suggestion that sequestering of LPS by lipid particles may form an integral part of a humoral detoxification mechanism. Previous studies on the biological properties of isolated lipoproteins used differential ultracentrifugation to separate the major subclasses. To preserve the integrity of the lipoproteins, we have analyzed the LPS distribution, specificity, binding capacity, and kinetics of binding to lipoproteins in human whole blood or plasma by using high-performance gel permeation chromatography and fluorescent LPS of three different chemotypes. The average distribution of O111:B4, J5, or Re595 LPS in whole blood from 10 human volunteers was 60% (+/-8%) high-density lipoprotein (HDL), 25% (+/-7%) low-density lipoprotein, and 12% (+/-5%) very low density lipoprotein. The saturation capacity of lipoproteins for all three LPS chemotypes was in excess of 200 microg/ml. Kinetic analysis however, revealed a strict chemotype dependence. The binding of Re595 or J5 LPS was essentially complete within 10 min, and subsequent redistribution among the lipoprotein subclasses occurred to attain similar distributions as O111:B4 LPS at 40 min. We conclude that under simulated physiological conditions, the binding of LPS to lipoproteins is highly specific, HDL has the highest binding capacity for LPS, the saturation capacity of lipoproteins for endotoxin far exceeds the LPS concentrations measured in clinical situations, and the kinetics of LPS association with lipoproteins display chemotype-dependent differences.

Indexed as

Chromatography, GelHumansKineticsLipopolysaccharidesLipoproteinsLipoproteins, HDLLipoproteins, LDLLipoproteins, VLDLLipopolysaccharidesLipoproteinsLipoproteins, HDLLipoproteins, LDLLipoproteins, VLDL

Identifiers

PMID11292694
PMCPMC98230
OpenAlexW2096137537

What OpenQuestion holds

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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.