Evidence map›Paper›PMID 18704198›Full record

ArticleThe Journal of clinical investigation2008

Drosophila are protected from Pseudomonas aeruginosa lethality by transgenic expression of paraoxonase-1.

David A Stoltz, Egon A Ozer, Peter J Taft, Marilyn Barry, Lei Liu, Peter J Kiss, Thomas O Moninger, Matthew R Parsek, Joseph Zabner

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

43 citing papers in PubMed, 81 citations in OpenAlex.

  1. Calprotectin protectsmSystems · 2025
    Article
  2. Review
  3. Review
  4. Thermostable Lactonases InhibitInternational journal of molecular sciences · 2023
    Article
  5. Infection and immunity · 2023
    Review
  6. Article
  7. Review
  8. Pseudomonas aeruginosa Quorum Sensing.Advances in experimental medicine and biology · 2022
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Host modification of a bacterial quorum-sensing signal induces a phenotypic switch in bacterial symbionts.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  16. Paraoxonases-1, -2 and -3: What are their functions?Chemico-biological interactions · 2016
    Article
  17. Article
  18. Review
  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

9 authors at 4 institutions in 1 country.

David A StoltzDepartment of Internal Medicine, University of Iowa, Carver College of Medicine, Iowa City, Iowa 52242, USA.
Egon A Ozer
Peter J Taft
Marilyn Barry
Lei Liu
Peter J Kiss
Thomas O Moninger
Matthew R Parsek
Joseph Zabner
University of Iowa · USOffice of Infectious Diseases · USTufts University · USUniversity of Washington · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007337 · NIGMS · UNIVERSITY OF IOWA · PI GEYER, PAMELA K., LENTZ, STEVEN R · 1985 to 2020
$15.9M
Paraoxonase-2 S311C Polymorphism Alters Glycosylation and Lactonase ActivityK08AI076671 · NIAID · UNIVERSITY OF IOWA · PI STOLTZ, DAVID A · 2008 to 2011
$605k
NIAID NIH HHS AI076671NIAID NIH HHS K08 AI076671NIGMS NIH HHS T32 GM007337PHS HHS 61234-09
6 · The paper itself

Abstract

Pseudomonas aeruginosa uses quorum sensing, an interbacterial communication system, to regulate gene expression. The signaling molecule N-3-oxododecanoyl homoserine lactone (3OC12-HSL) is thought to play a central role in quorum sensing. Since 3OC12-HSL can be degraded by paraoxonase (PON) family members, we hypothesized that PONs regulate P. aeruginosa virulence in vivo. We chose Drosophila melanogaster as our model organism because it has been shown to be a tractable model for investigating host-pathogen interactions and lacks PONs. By using quorum-sensing-deficient P. aeruginosa, synthetic acyl-HSLs, and transgenic expression of human PON1, we investigated the role of 3OC12-HSL and PON1 on P. aeruginosa virulence. We found that P. aeruginosa virulence in flies was dependent upon 3OC12-HSL. PON1 transgenic flies expressed enzymatically active PON1 and thereby exhibited arylesterase activity and resistance to organophosphate toxicity. Moreover, PON1 flies were protected from P. aeruginosa lethality, and protection was dependent on the lactonase activity of PON1. Our findings show that PON1 can interfere with quorum sensing in vivo and provide insight into what we believe is a novel role for PON1 in the innate immune response to quorum-sensing-dependent pathogens. These results raise intriguing possibilities about human-pathogen interactions, including potential roles for PON1 as a modifier gene and for PON1 protein as a regulator of normal bacterial florae, a link between infection/inflammation and cardiovascular disease, and a potential therapeutic modality.

Indexed as

Gene Expression Regulation, EnzymologicTransgenesAnimalsAnimals, Genetically ModifiedAryldialkylphosphataseDrosophila melanogasterImmunity, InnateInflammationModels, BiologicalModels, GeneticMutationPseudomonas aeruginosaPseudomonas InfectionsTime FactorsVirulenceAryldialkylphosphatase

Identifiers

PMID18704198
PMCPMC2515384
OpenAlexW2145154276

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.