Evidence map›Paper›PMID 28013162›Full record

ReviewCurrent opinion in microbiology2017

Bacteria and endothelial cells: a toxic relationship.

Ashira Lubkin, Victor J Torres

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

34 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Sympathetic regulation of the host immune response to bacterial sepsis.Clinical science (London, England : 1979) · 2025
    Review
  7. Article
  8. Article
  9. Monoclonal antibody neutralizesInfection and immunity · 2025
    Article
  10. Article
  11. Mechanisms of lung endothelial cell injury and survival in pulmonary arterial hypertension.American journal of physiology. Lung cellular and molecular physiology · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. IsMultiple sclerosis (Houndmills, Basingstoke, England) · 2023
    Review
  16. Article
  17. Review
  18. Review
  19. Frontiers in molecular biosciences · 2022
    Article
  20. 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

2 authors at 1 institution in 1 country.

Ashira LubkinDepartment of Microbiology, New York University School of Medicine, New York, NY 10016, United States.
Victor J TorresDepartment of Microbiology, New York University School of Medicine, New York, NY 10016, United States. Electronic address: victor.torres@nyumc.org.
New York University · US

Funding

MEDICAL SCIENTIST TRAININGT32GM007308 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI PHILIPS, MARK REID · 1985 to 2019
$23.2M
INFECTIOUS DISEASES &BASIC MICROBIOLOGICAL MECHANISMST32AI007180 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WEISER, JEFFREY NEAL · 1985 to 2022
$8.9M
Mechanistic Studies Of The Staphylococcus aureus LukAB CytotoxinR01AI099394 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Victor J. Torres · 2013 to 2026
$6.1M
Redefining the role of autophagy in bacterial diseaseR01AI121244 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI Ken Hashigiwa Cadwell · 2017 to 2026
$5.6M
Contribution of LukED to Staphylococcus aureus pathobiologyR01AI105129 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI TORRES, VICTOR J. · 2014 to 2023
$4.9M
Non-Leukocidal Roles of Staphylococcus aureus Bi-component toxins in PathogenesisF30AI124606 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI LUBKIN, ASHIRA LEAH · 2016 to 2019
$155k
NIAID NIH HHS F30 AI124606NIAID NIH HHS R01 AI099394NIAID NIH HHS R01 AI105129NIAID NIH HHS R01 AI121244NIAID NIH HHS T32 AI007180NIGMS NIH HHS T32 GM007308
6 · The paper itself

Abstract

Pathogenic bacteria use the bloodstream as a highway for getting around the body, and thus have to find ways to enter and exit through the endothelium. Many bacteria approach this problem by producing toxins that can breach the endothelial barrier through diverse creative mechanisms, including directly killing endothelial cells (ECs), weakening the cytoskeleton within ECs, and breaking the junctions between ECs. Toxins can also modulate the immune response by influencing endothelial biology, and can modulate endothelial function by influencing the response of leukocytes. Understanding these interactions, in both the in vitro and in vivo contexts, is of critical importance for designing new therapies for sepsis and other severe bacterial diseases.

Indexed as

AnimalsBacterial InfectionsBacterial ToxinsCytoplasmic VesiclesEndothelial CellsEndothelium, VascularGram-Negative BacteriaHumansMiceSepsisStaphylococcus aureusBacterial Toxins

Identifiers

PMID28013162
PMCPMC5481510
OpenAlexW2564806342

What OpenQuestion holds

Textmetadata
LicenceTDM
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.