Evidence map›Paper›PMID 41563930›Full record

ArticleJournal of innate immunity2026

Inhibition of <italic>Pseudomonas aeruginosa</italic> Biofilm Formation by Peptidyl-Arginine Deiminases 2 and 4.

Rory Baird, Debananda Gogoi, Luke Forde, Sara Waqas Ahmed, Mengxin Niu, Brenton Cavanagh, Fidelma Fitzpatrick, Emer P Reeves

Abstract read
In one paragraph

Article in Journal of innate immunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Rory BairdPulmonary Clinical Science, Department of Anaesthesia and Critical Care Medicine, RCSI University of Medicine and Health Sciences, Beaumont Hospital, Dublin, Ireland, rorybaird22@rcsi.ie.
Debananda GogoiPulmonary Clinical Science, Department of Anaesthesia and Critical Care Medicine, RCSI University of Medicine and Health Sciences, Beaumont Hospital, Dublin, Ireland.
Luke FordePulmonary Clinical Science, Department of Anaesthesia and Critical Care Medicine, RCSI University of Medicine and Health Sciences, Beaumont Hospital, Dublin, Ireland.
Sara Waqas AhmedPulmonary Clinical Science, Department of Anaesthesia and Critical Care Medicine, RCSI University of Medicine and Health Sciences, Beaumont Hospital, Dublin, Ireland.
Mengxin NiuPulmonary Clinical Science, Department of Anaesthesia and Critical Care Medicine, RCSI University of Medicine and Health Sciences, Beaumont Hospital, Dublin, Ireland.
Brenton CavanaghCellular and Molecular Imaging Core, RCSI University of Medicine and Health Sciences, Dublin, Ireland.
Fidelma FitzpatrickDepartment of Clinical Microbiology, Royal College of Surgeons in Ireland, Dublin, Ireland.
Emer P ReevesPulmonary Clinical Science, Department of Anaesthesia and Critical Care Medicine, RCSI University of Medicine and Health Sciences, Beaumont Hospital, Dublin, Ireland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionPseudomonas aeruginosa is a significant pathogen associated with acute and chronic infections, particularly in immunocompromised individuals. Its capacity for biofilm formation, combined with antibiotic resistance, plays a critical role in the persistence of these infections. Peptidyl-arginine deiminases (PADs), including PAD2 and PAD4 isoforms, are involved in neutrophil phagocytic killing of P. aeruginosa. This study aimed to investigate the impact of PAD enzymes on biofilm development and virulence factor production in P. aeruginosa, with focus on the multidrug resistant strain, PGO2330.

methodsBiofilm formation was assessed using crystal violet assays and confocal scanning laser microscopy. Quorum sensing (QS) gene expression and QS-related virulence factor production were quantified using qPCR and virulence factor assays.

resultsExposure to 20 n<sc>m</sc> of PAD2 or PAD4 reduced PGO2330 surface attachment (p < 0.0001) and biofilm formation to 67.9 ± 5.6% (p < 0.0001) and 68.2 ± 4.2% (p = 0.0004), respectively. Moreover, rPAD2 and rPAD4 citrullinated multiple protein substrates of P. aeruginosa, yet citrullination activity was not required by rPADs to reduce P. aeruginosa biofilm formation. PGO2330 exposed to PAD2 and PAD4 showed reduced lasR, lasI, rhlR, rhlI, and mvfR gene expression and reduced levels of extracellular DNA, rhamnolipids, pyocyanin, and protease activity.

conclusionThese results demonstrate that PADs inhibit P. aeruginosa biofilm formation and decrease the production of QS-related virulence factors, highlighting their potential as novel antimicrobials and supporting further research into the development of PAD-based therapeutics.

Indexed as

BiofilmsProtein-Arginine DeiminasesProtein-Arginine Deiminase Type 2Protein-Arginine Deiminase Type 4Pseudomonas aeruginosaPseudomonas InfectionsBacterial ProteinsGene Expression Regulation, BacterialHumansNeutrophilsQuorum SensingVirulence FactorsBacterial ProteinsProtein-Arginine DeiminasesProtein-Arginine Deiminase Type 2Protein-Arginine Deiminase Type 4Virulence FactorsBiofilmPeptidyl-arginine deiminase enzymesPseudomonas aeruginosaQuorum sensing molecules

Identifiers

PMID41563930
PMCPMC12948390

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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.