Evidence map›Paper›PMID 38646937›Full record

ArticleJCI insight2024

CETP inhibition enhances monocyte activation and bacterial clearance and reduces streptococcus pneumonia-associated mortality in mice.

Haoyu Deng, Wan Yi Liang, Le Qi Chen, Tin Ho Yuen, Basak Sahin, Dragoș M Vasilescu, Mark Trinder, Keith Walley, Patrick C.N. Rensen, John H Boyd and 1 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.6field-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

12 citing papers in PubMed, 12 citations in OpenAlex.

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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

11 authors at 3 institutions in 2 countries.

Haoyu DengDepartment of Medicine, Faculty of Medicine.
Wan Yi LiangDepartment of Microbiology and Immunology, Faculty of Science, and.
Le Qi ChenDepartment of Microbiology and Immunology, Faculty of Science, and.
Tin Ho YuenDepartment of Microbiology and Immunology, Faculty of Science, and.
Basak SahinCentre for Heart and Lung Innovation, St. Paul's Hospital.
Dragoș M VasilescuCentre for Heart and Lung Innovation, St. Paul's Hospital.
Mark TrinderCentre for Heart and Lung Innovation, St. Paul's Hospital.
Keith WalleyCentre for Heart and Lung Innovation, St. Paul's Hospital.
Patrick C.N. RensenDepartment of Medicine, Division of Endocrinology, and.
John H BoydDepartment of Medicine, Faculty of Medicine.
Liam R BrunhamDepartment of Medicine, Faculty of Medicine.
St. Paul's Hospital · CALeiden University Medical Center · NLUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is a leading cause of mortality worldwide, and pneumonia is the most common cause of sepsis in humans. Low levels of high-density lipoprotein cholesterol (HDL-C) levels are associated with an increased risk of death from sepsis, and increasing levels of HDL-C by inhibition of cholesteryl ester transfer protein (CETP) decreases mortality from intraabdominal polymicrobial sepsis in APOE*3-Leiden.CETP mice. Here, we show that treatment with the CETP inhibitor (CETPi) anacetrapib reduced mortality from Streptococcus pneumoniae-induced sepsis in APOE*3-Leiden.CETP and APOA1.CETP mice. Mechanistically, CETP inhibition reduced the host proinflammatory response via attenuation of proinflammatory cytokine transcription and release. This effect was dependent on the presence of HDL, leading to attenuation of immune-mediated organ damage. In addition, CETP inhibition promoted monocyte activation in the blood prior to the onset of sepsis, resulting in accelerated macrophage recruitment to the lung and liver. In vitro experiments demonstrated that CETP inhibition significantly promoted the activation of proinflammatory signaling in peripheral blood mononuclear cells and THP1 cells in the absence of HDL; this may represent a mechanism responsible for improved bacterial clearance during sepsis. These findings provide evidence that CETP inhibition represents a potential approach to reduce mortality from pneumosepsis.

Indexed as

Cholesterol Ester Transfer ProteinsMonocytesStreptococcus pneumoniaeAnimalsApolipoprotein E3Cholesterol, HDLDisease Models, AnimalFemaleHumansMacrophagesMicePneumonia, PneumococcalSepsisTHP-1 CellsApolipoprotein E3CETP protein, humanCholesterol Ester Transfer ProteinsCholesterol, HDLBacterial infectionsCardiologyInfectious diseaseLipoproteins

Identifiers

PMID38646937
PMCPMC11141867
OpenAlexW4395049682

What OpenQuestion holds

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LicenceCC BY
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.