Evidence map›Paper›PMID 27481727›Full record

ArticlePathogens and disease2016

Signaling events in pathogen-induced macrophage foam cell formation.

Yazdani B Shaik-Dasthagirisaheb, Samrawit Mekasha, Xianbao He, Frank C Gibson, Robin R Ingalls

Open access · bronzeAbstract read
In one paragraph

Article in Pathogens and disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. The ethanol extract ofFrontiers in cardiovascular medicine · 2022
    Article
  4. Role of Macrophages and RhoA Pathway in Atherosclerosis.International journal of molecular sciences · 2020
    Review
  5. Oral PathogenMicroorganisms · 2020
    Article
  6. Article
  7. Review
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

5 authors at 2 institutions in 1 country.

Yazdani B Shaik-DasthagirisahebSection of Infectious Diseases, Department of Medicine, Boston Medical Center and Boston University School of Medicine, Boston, MA 02118, USA.
Samrawit MekashaSection of Infectious Diseases, Department of Medicine, Boston Medical Center and Boston University School of Medicine, Boston, MA 02118, USA.
Xianbao HeSection of Infectious Diseases, Department of Medicine, Boston Medical Center and Boston University School of Medicine, Boston, MA 02118, USA.
Frank C GibsonSection of Infectious Diseases, Department of Medicine, Boston Medical Center and Boston University School of Medicine, Boston, MA 02118, USA.
Robin R IngallsSection of Infectious Diseases, Department of Medicine, Boston Medical Center and Boston University School of Medicine, Boston, MA 02118, USA ringalls@bu.edu.
Boston University · USBoston Medical Center · US

Funding

Role of Innate Immune System in Pathogen Induced Chronic InflammationP01AI078894 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GENCO, CAROLINE A · 2010 to 2014
$7.4M
PPARs and periodontal diseaseR21DE024275 · NIDCR · UNIVERSITY OF FLORIDA · PI GIBSON, FRANK C · 2015 to 2016
$479k
NIAID NIH HHS P01 AI078894NIDCR NIH HHS R21 DE024275
6 · The paper itself

Abstract

Macrophage foam cell formation is a key event in atherosclerosis. Several triggers induce low-density lipoprotein (LDL) uptake by macrophages to create foam cells, including infections with Porphyromonas gingivalis and Chlamydia pneumoniae, two pathogens that have been linked to atherosclerosis. While gene regulation during foam cell formation has been examined, comparative investigations to identify shared and specific pathogen-elicited molecular events relevant to foam cell formation are not well documented. We infected mouse bone marrow-derived macrophages with P. gingivalis or C. pneumoniae in the presence of LDL to induce foam cell formation, and examined gene expression using an atherosclerosis pathway targeted plate array. We found over 30 genes were significantly induced in response to both pathogens, including PPAR family members that are broadly important in atherosclerosis and matrix remodeling genes that may play a role in plaque development and stability. Six genes mainly involved in lipid transport were significantly downregulated. The response overall was remarkably similar and few genes were regulated in a pathogen-specific manner. Despite very divergent lifestyles, P. gingivalis and C. pneumoniae activate similar gene expression profiles during foam cell formation that may ultimately serve as targets for modulating infection-elicited foam cell burden, and progression of atherosclerosis.

Indexed as

Host-Pathogen InteractionsSignal TransductionAnimalsAtherosclerosisChlamydophila pneumoniaeCluster AnalysisComputational BiologyCytokinesFoam CellsGene Expression ProfilingGene OntologyImmunity, InnateInflammationInflammation MediatorsLipid MetabolismLipid PeroxidationCytokinesInflammation MediatorsatherosclerosisChlamydia pneumoniaefoam cellinnate immunitymacrophagePorphyromonas gingivalis

Identifiers

PMID27481727
PMCPMC5985511
OpenAlexW2500122758

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.