Evidence map›Paper›PMID 39840902›Full record

ArticleJournal of extracellular vesicles2025

Uncovering a new family of conserved virulence factors that promote the production of host-damaging outer membrane vesicles in gram-negative bacteria.

Audrey Goman, Bérengère Ize, Katy Jeannot, Camille Pin, Delphine Payros, Cécile Goursat, Léa Ravon-Katossky, Kazunori Murase, Camille V Chagneau, Hélène Revillet and 6 more

Abstract read
In one paragraph

Article in Journal of extracellular vesicles, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Targeting Outer Membrane Vesicles ofJournal of microbiology and biotechnology · 2026
    Review
  2. Review
  3. Review
  4. Review
  5. StudyingMicrobiology spectrum · 2025
    Article
  6. Article
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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

16 authors.

Audrey GomanInstitut de Recherche en Santé Digestive (IRSD), Université de Toulouse, INSERM, INRAE, ENVT, UPS, Toulouse, France.ORCID https://orcid.org/0009-0002-6782-7144
Bérengère IzeLaboratoire d'Ingénierie des Systèmes Macromoléculaires (LISM-UMR7255), Institut de Microbiologie de la Méditerannée (IMM), Aix-Marseille Université, Centre National de la Recherche Scientifique, Marseille, France.ORCID https://orcid.org/0000-0001-9106-9254
Katy JeannotCentre National de Référence de la Résistance aux Antibiotiques, Centre Hospitalier Universitaire de Besançon, Besançon, France.ORCID https://orcid.org/0000-0002-4634-8550
Camille PinInstitut de Recherche en Santé Digestive (IRSD), Université de Toulouse, INSERM, INRAE, ENVT, UPS, Toulouse, France.ORCID https://orcid.org/0000-0002-3310-6309
Delphine PayrosInstitut de Recherche en Santé Digestive (IRSD), Université de Toulouse, INSERM, INRAE, ENVT, UPS, Toulouse, France.ORCID https://orcid.org/0000-0003-4820-7986
Cécile GoursatInstitut de Recherche en Santé Digestive (IRSD), Université de Toulouse, INSERM, INRAE, ENVT, UPS, Toulouse, France.
Léa Ravon-KatosskyInstitut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, UPS, Toulouse, France.
Kazunori MuraseDepartment of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID https://orcid.org/0000-0002-7202-4357
Camille V ChagneauInstitut de Recherche en Santé Digestive (IRSD), Université de Toulouse, INSERM, INRAE, ENVT, UPS, Toulouse, France.ORCID https://orcid.org/0000-0002-3061-9184
Hélène RevilletInstitut de Recherche en Santé Digestive (IRSD), Université de Toulouse, INSERM, INRAE, ENVT, UPS, Toulouse, France.ORCID https://orcid.org/0000-0001-8427-4110
Frédéric TaiebInstitut de Recherche en Santé Digestive (IRSD), Université de Toulouse, INSERM, INRAE, ENVT, UPS, Toulouse, France.ORCID https://orcid.org/0000-0001-9612-2069
Sophie BlevesLaboratoire d'Ingénierie des Systèmes Macromoléculaires (LISM-UMR7255), Institut de Microbiologie de la Méditerannée (IMM), Aix-Marseille Université, Centre National de la Recherche Scientifique, Marseille, France.ORCID https://orcid.org/0000-0002-9406-3437
Laure DavidInstitut de Recherche en Santé Digestive (IRSD), Université de Toulouse, INSERM, INRAE, ENVT, UPS, Toulouse, France.ORCID https://orcid.org/0000-0003-0339-4941
Etienne MeunierInstitut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, UPS, Toulouse, France.ORCID https://orcid.org/0000-0002-3651-4877
Priscilla BranchuInstitut de Recherche en Santé Digestive (IRSD), Université de Toulouse, INSERM, INRAE, ENVT, UPS, Toulouse, France.ORCID https://orcid.org/0000-0002-8127-1181
Eric OswaldInstitut de Recherche en Santé Digestive (IRSD), Université de Toulouse, INSERM, INRAE, ENVT, UPS, Toulouse, France.ORCID https://orcid.org/0000-0002-3017-0081

Funding

Agence Nationale de la Recherche ANR-20-CE18-0016Agence Nationale de la Recherche ANR-20-CE44-0017Agence Nationale de la Recherche ANR-21-CE21-0006-01_ACTAgence Nationale de la Recherche ANR-23-CE14-0070-01Agence Nationale de la Recherche ANR-23-CE44-0018-03Université Toulouse III - Paul Sabatier AO Tremplin UT3 PIME-ID
6 · The paper itself

Abstract

CprA is a short-chain dehydrogenase/reductase (SDR) that contributes to resistance against colistin and antimicrobial peptides. The cprA gene is conserved across Pseudomonas aeruginosa clades and its expression is directly regulated by the two-component system PmrAB. We have shown that cprA expression leads to the production of outer membrane vesicles (OMVs) that block autophagic flux and have a greater capacity to activate the non-canonical inflammasome pathway. In a murine model of sepsis, a P. aeruginosa strain deleted for cprA was less virulent than the wild-type (WT) strain. These results demonstrate the important role of CprA in the pathogenicity of P. aeruginosa. It is worth noting that CprA is also a functional ortholog of hemolysin F (HlyF), which is encoded by virulence plasmids of Escherichia coli. We have shown that other cryptic SDRs encoded by mammalian and plant pathogens, such as Yersinia pestis and Ralstonia solanacearum are functional orthologs of CprA and HlyF. These SDRs also induce the production of OMVs which block autophagic flux. This study uncovers a new family of virulence determinants in Gram-negative bacteria, offering potential for innovative therapeutic interventions and deeper insights into bacterial pathogenesis.

Indexed as

Bacterial Outer MembraneExtracellular VesiclesGram-Negative BacteriaPseudomonas aeruginosaVirulence FactorsAnimalsBacterial ProteinsHumansMiceVirulenceBacterial ProteinsVirulence FactorsautophagyinflammasomeOMVspathogenicityPmrABpolymyxinsPseudomonas aeruginosa

Identifiers

PMID39840902
PMCPMC11752146

What Socratic 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 Socratic graph.