Evidence map›Paper›PMID 27329564›Full record

ArticleImmunology2016

High-density lipoprotein reduces inflammation from cholesterol crystals by inhibiting inflammasome activation.

Seth G Thacker, Abdalrahman Zarzour, Ye Chen, Mustafa S Alcicek, Lita A Freeman, Dennis O Sviridov, Stephen J Demosky, Alan T Remaley

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 2 pooled it
4.5field-weighted citation impact, top 5% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

82 citing papers in PubMed, 2 syntheses or guidelines pooled it, 126 citations in OpenAlex.

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22 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

8 authors at 2 institutions in 1 country.

Seth G ThackerLipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Abdalrahman ZarzourLipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Ye ChenSystems Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Mustafa S AlcicekLipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Lita A FreemanLipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Dennis O SviridovLipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Stephen J DemoskyLipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Alan T RemaleyLipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. aremaley1@nhlbi.nih.gov.
National Heart Lung and Blood Institute · USNational Institutes of Health · US

Funding

NHLBI Animal Program DivisionZIGHL006020 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI CLARK, TANNIA · 2009 to 2025
$47.3M
Use Of Animal Models To Study Lipid Genes That Modulate AtherosclerosisZIAHL002058 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI REMALEY, ALAN THOMAS · 2009 to 2019
$14.3M
Systems Biology CoreZIAHL006192 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI WANG, XUJING · 2014 to 2016
$4.6M
6 · The paper itself

Abstract

Interleukin-1β (IL-1β), a potent pro-inflammatory cytokine, has been implicated in many diseases, including atherosclerosis. Activation of IL-1β is controlled by a multi-protein complex, the inflammasome. The exact initiating event in atherosclerosis is unknown, but recent work has demonstrated that cholesterol crystals (CC) may promote atherosclerosis development by activation of the inflammasome. High-density lipoprotein (HDL) has consistently been shown to be anti-atherogenic and to have anti-inflammatory effects, but its mechanism of action is unclear. We demonstrate here that HDL is able to suppress IL-1β secretion in response to cholesterol crystals in THP-1 cells and in human-monocyte-derived macrophages. HDL is able to blunt inflammatory monocyte cell recruitment in vivo following intraperitoneal CC injection in mice. HDL appears to modulate inflammasome activation in several ways. It reduces the loss of lysosomal membrane integrity following the phagocytosis of CC, but the major mechanism for the suppression of inflammasome activation by HDL is decreased expression of pro-IL-1β and NLRP3, and reducing caspase-1 activation. In summary, we have described a novel anti-inflammatory effect of HDL, namely its ability to suppress inflammasome activation by CC by modulating the expression of several key components of the inflammasome.

Indexed as

AnimalsAnti-Inflammatory AgentsAtherosclerosisCell LineCholesterolFemaleHumansInflammasomesInflammationInterleukin-1betaLipoproteins, HDLMacrophagesMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinAnti-Inflammatory AgentsCholesterolInflammasomesInterleukin-1betaLipoproteins, HDLNLR Family, Pyrin Domain-Containing 3 Proteinapolipoprotein A Ihigh-density lipoproteininflammasomeinterleukin-1β

Identifiers

PMID27329564
PMCPMC5046053
OpenAlexW2462040401

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.