Evidence map›Paper›PMID 23166496›Full record

ArticlePLoS pathogens2012

The quorum sensing volatile molecule 2-amino acetophenon modulates host immune responses in a manner that promotes life with unwanted guests.

Arunava Bandyopadhaya, Meenu Kesarwani, Yok-Ai Que, Jianxin He, Katie Padfield, Ronald Tompkins, Laurence G Rahme

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2012. 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
2.0field-weighted citation impact, top 13% 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, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. Molecular Mechanisms Underlying the Pathogenicity ofMedicina (Kaunas, Lithuania) · 2026
    Review
  4. Frontiers in immunology · 2025
    Review
  5. Revealing the impact ofFrontiers in immunology · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Animal Models for Pseudomonas aeruginosa Quorum Sensing Studies.Methods in molecular biology (Clifton, N.J.) · 2018
    Article
  18. Article
  19. Review
  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

7 authors at 3 institutions in 1 country.

Arunava BandyopadhayaDepartment of Surgery, Harvard Medical School and Massachusetts General Hospital, Boston, Massachusetts, United States of America.
Meenu Kesarwani
Yok-Ai Que
Jianxin He
Katie Padfield
Ronald Tompkins
Laurence G Rahme
Harvard University · USShriners Hospitals for Children - Boston · USMassachusetts General Hospital · US

Funding

Interruption of Signaling-Mediated Bacterial Persistent InfectionsR33AI105902 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI RAHME, LAURENCE G · 2015 to 2017
$1.8M
Interruption of Signaling-Mediated Bacterial Persistent InfectionsR21AI105902 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI RAHME, LAURENCE G · 2013 to 2014
$478k
NIAID NIH HHS R21 AI105902NIAID NIH HHS R33 AI105902
6 · The paper itself

Abstract

Increasing evidence indicates that bacterial quorum sensing (QS) signals are important mediators of immunomodulation. However, whether microbes utilize these immunomodulatory signals to maintain infection remain unclear. Here, we show that the Pseudomonas aeruginosa QS-regulated molecule 2-amino acetophenone (2-AA) modulates host immune responses in a manner that increases host ability to cope with this pathogen. Mice treated with 2-AA prior to infection had a 90% survival compared to 10% survival rate observed in the non-pretreated infected mice. Whilst 2-AA stimulation activates key innate immune response pathways involving mitogen-activated protein kinases (MAPKs), nuclear factor (NF)-κB, and pro-inflammatory cytokines, it attenuates immune response activation upon pretreatment, most likely by upregulating anti-inflammatory cytokines. 2-AA host pretreatment is characterized by a transcriptionally regulated block of c-JUN N-terminal kinase (JNK) and NF-κB activation, with relatively preserved activation of extracellular regulated kinase (ERK) 1/2. These kinase changes lead to CCAAT/enhancer-binding protein-β (c/EBPβ) activation and formation of the c/EBPβ-p65 complex that prevents NF-κB activation. 2-AA's aptitude for dampening the inflammatory processes while increasing host survival and pathogen persistence concurs with its ability to signal bacteria to switch to a chronic infection mode. Our results reveal a QS immunomodulatory signal that promotes original aspects of interkingdom communication. We propose that this communication facilitates pathogen persistence, while enabling host tolerance to infection.

Indexed as

AcetophenonesAnimalsCCAAT-Enhancer-Binding Protein-betaCell LineCytokinesImmunity, InnateImmunologic FactorsMAP Kinase Kinase 4MiceMitogen-Activated Protein Kinase 3Pseudomonas aeruginosaPseudomonas InfectionsQuorum SensingTranscription Factor RelA2-aminoacetophenoneAcetophenonesCCAAT-Enhancer-Binding Protein-betaCytokinesImmunologic FactorsMAP Kinase Kinase 4Mitogen-Activated Protein Kinase 3Rela protein, mouseTranscription Factor RelA

Identifiers

PMID23166496
PMCPMC3499575
OpenAlexW2138666939

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.