Evidence map›Paper›PMID 26785849›Full record

ArticleScientific reports2016

Biophysical regulation of Chlamydia pneumoniae-infected monocyte recruitment to atherosclerotic foci.

Shankar J Evani, Anand K Ramasubramanian

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
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  9. Article
  10. Manipulation of Host Cholesterol by Obligate Intracellular Bacteria.Frontiers in cellular and infection microbiology · 2017
    Review
  11. Review
  12. Article
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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

2 authors at 1 institution in 1 country.

Shankar J EvaniDepartment of Biomedical Engineering, University of Texas at San Antonio, San Antonio, TX 78249, USA.
Anand K RamasubramanianDepartment of Biomedical Engineering, University of Texas at San Antonio, San Antonio, TX 78249, USA.
The University of Texas at San Antonio · US

Funding

RCMI Center for Interdiscplinary Health Research CIHRG12MD007591 · NIMHD · UNIVERSITY OF TEXAS SAN ANTONIO · PI PERRY, GEORGE · 2012 to 2016
$10.4M
Role of fluid flow on Chlamydia pneumoniae-exacerbated atherosclerosisSC1HL112629 · NHLBI · UNIVERSITY OF TEXAS SAN ANTONIO · PI RAMASUBRAMANIAN, ANAND K · 2011 to 2015
$1.8M
NHLBI NIH HHS HL112629NHLBI NIH HHS SC1 HL112629NIMHD NIH HHS G12 MD007591NIMHD NIH HHS G12MD007591
6 · The paper itself

Abstract

Chlamydia pneumoniae infection is implicated in atherosclerosis although the contributory mechanisms are poorly understood. We hypothesize that C. pneumoniae infection favors the recruitment of monocytes to atherosclerotic foci by altering monocyte biophysics. Primary, fresh human monocytes were infected with C. pneumoniae for 8 h, and the interactions between monocytes and E-selectin or aortic endothelium under flow were characterized by video microscopy and image analysis. The distribution of membrane lipid rafts and adhesion receptors were analyzed by imaging flow cytometry. Infected cells rolled on E-selectin and endothelial surfaces, and this rolling was slower, steady and uniform compared to uninfected cells. Infection decreases cholesterol levels, increases membrane fluidity, disrupts lipid rafts, and redistributes CD44, which is the primary mediator of rolling interactions. Together, these changes translate to higher firm adhesion of infected monocytes on endothelium, which is enhanced in the presence of LDL. Uninfected monocytes treated with LDL or left untreated were used as baseline control. Our results demonstrate that the membrane biophysical changes due to infection and hyperlipidemia are one of the key mechanisms by which C. pneumoniae can exacerbate atherosclerotic pathology. These findings provide a framework to characterize the role of 'infectious burden' in the development and progression of atherosclerosis.

Indexed as

Biophysical PhenomenaChemotaxisAtherosclerosisCell AdhesionChlamydophila pneumoniaeCholesterol, LDLEndothelium, VascularE-SelectinHumansHyaluronan ReceptorsLeukocyte RollingMembrane FluidityMembrane MicrodomainsMonocytesPlaque, AtheroscleroticCholesterol, LDLE-SelectinHyaluronan Receptors

Identifiers

PMID26785849
PMCPMC4726309
OpenAlexW2434037029

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.