Evidence map›Paper›PMID 25183769›Full record

ArticleThe Journal of infectious diseases2015

Pneumococcal hydrogen peroxide-induced stress signaling regulates inflammatory genes.

Maria Loose, Martina Hudel, Klaus-Peter Zimmer, Ernesto Garcia, Sven Hammerschmidt, Rudolf Lucas, Trinad Chakraborty, Helena Pillich

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Contribution of Puma to Inflammatory Resolution During Early Pneumococcal Pneumonia.Frontiers in cellular and infection microbiology · 2022
    Article
  5. Review
  6. Review
  7. Toxins · 2021
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Mitochondrial DNA Leakage Caused byFrontiers in microbiology · 2019
    Article
  13. Article
  14. Frontiers in immunology · 2018
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

8 authors at 5 institutions in 3 countries.

Maria LooseInstitute for Medical Microbiology, German Center for Infection Giessen-Marburg-Langen Site.
Martina HudelInstitute for Medical Microbiology, German Center for Infection Giessen-Marburg-Langen Site.
Klaus-Peter ZimmerDepartment of Pediatrics, Justus-Liebig University, Giessen.
Ernesto GarciaCentro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas, and Centro de Investigación Biomédica en Red de Enfermedades Respiratorias, Madrid, Spain.
Sven HammerschmidtDepartment Genetics of Microorganisms, Interfaculty Institute for Genetics and Functional Genomics, Ernst Moritz Arndt University of Greifswald, Germany.
Rudolf LucasVascular Biology Center, Department of Pharmacology and Toxicology, Georgia Health Sciences University, Augusta.
Trinad ChakrabortyInstitute for Medical Microbiology, German Center for Infection Giessen-Marburg-Langen Site.
Helena PillichInstitute for Medical Microbiology, German Center for Infection Giessen-Marburg-Langen Site.
German Center for Infection Research · DEAugusta University Health · USCentro de Investigaciones Biológicas Margarita Salas · ESJustus-Liebig-Universität Gießen · DEUniversität Greifswald · DE

Funding

Protective activity of the lectin-like domain of TNF in permeability edemaR01HL094609 · NHLBI · AUGUSTA UNIVERSITY · PI LUCAS, RUDOLF · 2010 to 2013
$1.5M
NHLBI NIH HHS R01 HL094609NHLBI NIH HHS R01HL094609
6 · The paper itself

Abstract

Microbial infections can induce aberrant responses in cellular stress pathways, leading to translational attenuation, metabolic restriction, and activation of oxidative stress, with detrimental effects on cell survival. Here we show that infection of human airway epithelial cells with Streptococcus pneumoniae leads to induction of endoplasmic reticulum (ER) and oxidative stress, activation of mitogen-associated protein kinase (MAPK) signaling pathways, and regulation of their respective target genes. We identify pneumococcal H2O2 as the causative agent for these responses, as both catalase-treated and pyruvate oxidase-deficient bacteria lacked these activities. Pneumococcal H2O2 induced nuclear NF-κB translocation and transcription of proinflammatory cytokines. Inhibition of translational arrest and ER stress by salubrinal or of MAPK signaling pathways attenuate cytokine transcription. These results provide strong evidence for the notion that inhibition of translation is an important host pathway in monitoring harmful pathogen-associated activities, thereby enabling differentiation between pathogenic and nonpathogenic bacteria.

Indexed as

Host-Pathogen InteractionsInflammationStress, PhysiologicalCell LineCytokinesEpithelial CellsGene Expression RegulationHumansHydrogen PeroxideNF-kappa BSignal TransductionStreptococcus pneumoniaeCytokinesHydrogen PeroxideNF-kappa BER stresshydrogen peroxideimmune responseMAPKStreptococcus pneumonia

Identifiers

PMID25183769
PMCPMC4334831
OpenAlexW1991678384

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.