Evidence map›Paper›PMID 24452679›Full record

ArticleInfection and immunity2014

Induction of virulence gene expression in Staphylococcus aureus by pulmonary surfactant.

Kenichi Ishii, Tatsuo Adachi, Jyunichiro Yasukawa, Yutaka Suzuki, Hiroshi Hamamoto, Kazuhisa Sekimizu

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Lung surfactant reducesMicrobiology spectrum · 2025
    Article
  4. Review
  5. Bacterial acquisition of host fatty acids has far-reaching implications on virulence.Microbiology and molecular biology reviews : MMBR · 2024
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  10. Teicoplanin associated geneFrontiers in microbiology · 2023
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  11. Targeting the Achilles' Heel of Multidrug-ResistantInternational journal of molecular sciences · 2022
    Article
  12. The gene regulatory network ofFrontiers in microbiology · 2022
    Article
  13. The Type VII Secretion System ofAnnual review of microbiology · 2021
    Article
  14. Article
  15. Article
  16. Review
  17. Regulation ofMicrobiology spectrum · 2019
    Review
  18. Article
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  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

6 authors at 2 institutions in 1 country.

Kenichi IshiiGraduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo, Japan.
Tatsuo Adachi
Jyunichiro Yasukawa
Yutaka Suzuki
Hiroshi Hamamoto
Kazuhisa Sekimizu
The University of Tokyo · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We performed a genomewide analysis using a next-generation sequencer to investigate the effect of pulmonary surfactant on gene expression in Staphylococcus aureus, a clinically important opportunistic pathogen. RNA sequence (RNA-seq) analysis of bacterial transcripts at late log phase revealed 142 genes that were upregulated >2-fold following the addition of pulmonary surfactant to the culture medium. Among these genes, we confirmed by quantitative reverse transcription-PCR analysis that mRNA amounts for genes encoding ESAT-6 secretion system C (EssC), an unknown hypothetical protein (NWMN_0246; also called pulmonary surfactant-inducible factor A [PsiA] in this study), and hemolysin gamma subunit B (HlgB) were increased 3- to 10-fold by the surfactant treatment. Among the major constituents of pulmonary surfactant, i.e., phospholipids and palmitate, only palmitate, which is the most abundant fatty acid in the pulmonary surfactant and a known antibacterial substance, stimulated the expression of these three genes. Moreover, these genes were also induced by supplementing the culture with detergents. The induction of gene expression by surfactant or palmitate was not observed in a disruption mutant of the sigB gene, which encodes an alternative sigma factor involved in bacterial stress responses. Furthermore, each disruption mutant of the essC, psiA, and hlgB genes showed attenuation of both survival in the lung and host-killing ability in a murine pneumonia model. These findings suggest that S. aureus resists membrane stress caused by free fatty acids present in the pulmonary surfactant through the regulation of virulence gene expression, which contributes to its pathogenesis within the lungs of the host animal.

Indexed as

Staphylococcal InfectionsAnimalsBacterial ProteinsDisease Models, AnimalFemaleGene Expression ProfilingGene Expression Regulation, BacterialGenome-Wide Association StudyMicePulmonary SurfactantsReverse Transcriptase Polymerase Chain ReactionRNA, BacterialRNA, MessengerSequence Analysis, RNASigma FactorStaphylococcus aureusBacterial ProteinsPulmonary SurfactantsRNA, BacterialRNA, MessengerSigma Factor

Identifiers

PMID24452679
PMCPMC3993393
OpenAlexW2126610995

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.