Evidence map›Paper›PMID 25188225›Full record

ArticlePLoS pathogens2014

Mouse, but not human, ApoB-100 lipoprotein cholesterol is a potent innate inhibitor of Streptococcus pneumoniae pneumolysin.

Kristin R Wade, Eileen M Hotze, David E Briles, Rodney K Tweten

Open access · goldAbstract readComparative Study
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Effect of Total SMS Activity on LDL Catabolism in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2023
    Article
  5. Article
  6. Article
  7. Review
  8. Pneumolysin: Pathogenesis and Therapeutic Target.Frontiers in microbiology · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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 1 country.

Kristin R WadeDepartment of Microbiology and Immunology, The University of Oklahoma Sciences Center, Oklahoma City, Oklahoma, United States of America.
Eileen M HotzeDepartment of Microbiology and Immunology, The University of Oklahoma Sciences Center, Oklahoma City, Oklahoma, United States of America.
David E BrilesDepartment of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Rodney K TwetenDepartment of Microbiology and Immunology, The University of Oklahoma Sciences Center, Oklahoma City, Oklahoma, United States of America.
University of Oklahoma Health Sciences Center · USUniversity of Alabama at Birmingham · US

Funding

Pore Formation by Cholesterol Dependent CytolysinsR01AI037657 · NIAID · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI TWETEN, RODNEY K. · 1997 to 2015
$5.4M
Pore Formation by Cholesterol Dependent CytolysinsR37AI037657 · NIAID · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI TWETEN, RODNEY K. · 2016 to 2025
$4.8M
NIAID NIH HHS AI-37657NIAID NIH HHS R01 AI037657NIAID NIH HHS R37 AI037657
6 · The paper itself

Abstract

Streptococcus pneumoniae produces the pore-forming toxin pneumolysin (PLY), which is a member of the cholesterol-dependent cytolysin (CDC) family of toxins. The CDCs recognize and bind the 3β-hydroxyl group of cholesterol at the cell surface, which initiates membrane pore formation. The cholesterol transport lipoproteins, which carry cholesterol in their outer monolayer, are potential off-pathway binding targets for the CDCs and are present at significant levels in the serum and the interstitial spaces of cells. Herein we show that cholesterol carried specifically by the ApoB-100-containing lipoprotein particles (CH-ApoB-100) in the mouse, but not that carried by human or guinea pig particles, is a potent inhibitor of the PLY pore-forming mechanism. Cholesterol present in the outer monolayer of mouse ApoB-100 particles is recognized and bound by PLY, which stimulates premature assembly of the PLY oligomeric complex thereby inactivating PLY. These studies further suggest that the vast difference in the inhibitory capacity of mouse CH-ApoB-100 and that of the human and the guinea pig is due to differences in the presentation of cholesterol in the outer monolayer of their ApoB-100 particles. Therefore mouse CH-ApoB-100 represents a significant innate CDC inhibitor that is absent in humans, which may underestimate the contribution of CDCs to human disease when utilizing mouse models of disease.

Indexed as

AnimalsAntibodies, NeutralizingApolipoprotein B-100Bacterial ProteinsCell MembraneCholesterolGuinea PigsHemolysisHumansLipoproteinsMiceMice, Inbred BALB CMice, Inbred C57BLStreptolysinsAntibodies, NeutralizingApolipoprotein B-100Bacterial ProteinsCholesterollipoprotein cholesterolLipoproteinsplY protein, Streptococcus pneumoniaeStreptolysins

Identifiers

PMID25188225
PMCPMC4154877
OpenAlexW2027053173

What OpenQuestion holds

Textmetadata
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.