Evidence map›Paper›PMID 25667262›Full record

ArticleInfection and immunity2015

Role of copper efflux in pneumococcal pathogenesis and resistance to macrophage-mediated immune clearance.

Michael D L Johnson, Thomas E Kehl-Fie, Roger Klein, Jacqueline Kelly, Corinna Burnham, Beth Mann, Jason W Rosch

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
5.9field-weighted citation impact, top 4% 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

62 citing papers in PubMed, 82 citations in OpenAlex.

  1. Review
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  9. Review
  10. Improved diagnostic markers for invasive pulmonary aspergillosis in COPD patients.Frontiers in cellular and infection microbiology · 2024
    Article
  11. Article
  12. Article
  13. Mutations inApplied and environmental microbiology · 2023
    Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Infection and immunity · 2022
    Article
  20. Review

2 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Michael D L JohnsonDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Thomas E Kehl-FieUniversity of Illinois Urbana-Champaign, Department of Microbiology, Urbana, Illinois, USA.
Roger KleinDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Jacqueline KellyDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Corinna BurnhamDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Beth MannDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Jason W RoschDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA jason.rosch@stjude.org.
St. Jude Children's Research Hospital · USUniversity of Illinois Urbana-Champaign · US

Funding

PROFESSIONAL ONCOLOGY EDUCATION PROGRAMR25CA023944 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI SUZANNE A. GRONEMEYER · 1986 to 2026
$8.3M
Interdisciplinary Training Program in Lung ResearchT32HL094296 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Ray Stokes Peebles · 2008 to 2026
$6.3M
Pneumococcal pathogenesis in sickle cell diseaseR01AI110618 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI ROSCH, JASON W. · 2015 to 2019
$2.2M
Adaptation of Staphylococcus aureus to Mn and Zn starvation imposed by the hostK22AI104805 · NIAID · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI KEHL-FIE, THOMAS EVERETT · 2014 to 2015
$264k
NCI NIH HHS 5R25CA23944NCI NIH HHS R25 CA023944NHLBI NIH HHS T32 HL094296NIAID NIH HHS K22 AI104805NIAID NIH HHS K22AI104805-01NIAID NIH HHS R01 AI110618NIAID NIH HHS R01AI110618
6 · The paper itself

Abstract

In bacteria, the intracellular levels of metals are mediated by tightly controlled acquisition and efflux systems. This is particularly true of copper, a trace element that is universally toxic in excess. During infection, the toxic properties of copper are exploited by the mammalian host to facilitate bacterial clearance. To better understand the role of copper during infection, we characterized the contribution of the cop operon to copper homeostasis and virulence in Streptococcus pneumoniae. Deletion of either the exporter, encoded by copA, or the chaperone, encoded by cupA, led to hypersensitivity to copper stress. We further demonstrated that loss of the copper exporter encoded by copA led to decreased virulence in pulmonary, intraperitoneal, and intravenous models of infection. Deletion of copA resulted in enhanced macrophage-mediated bacterial clearance in vitro. The attenuation phenotype of the copA mutant in the lung was found to be dependent on pulmonary macrophages, underscoring the importance of copper efflux in evading immune defenses. Overall, these data provide insight into the role of the cop operon in pneumococcal pathogenesis.

Indexed as

AnimalsBacteremiaBacterial AdhesionBacterial ProteinsCation Transport ProteinsCell LineCopperGene DeletionGene Expression Regulation, BacterialHumansLungMacrophagesMiceMice, Inbred BALB CMolecular ChaperonesPneumococcal InfectionsBacterial ProteinsCation Transport ProteinsCopA protein, BacteriaCopperMolecular Chaperones

Identifiers

PMID25667262
PMCPMC4363445
OpenAlexW2051144562

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.