Evidence map›Paper›PMID 42919968›Full record

ArticleNature microbiology2026

FibriLysins disrupt Staphylococcus aureus biofilms and abscess communities.

Vincent De Maesschalck, Marco Chittò, Claudia Siverino, Lena Gens, Stephan Zeiter, Alisa Hangartner, Sandrine Harzé, Eliane Vanhoffelen, Camille Van Laere, Alison Kerremans and 9 more

Abstract read
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In one paragraph

Article in Nature microbiology, 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

19 authors.

Vincent De Maesschalck *Laboratory of Gene Technology, Department of Biosystems, KU Leuven, Leuven, Belgium.
Marco Chittò *AO Research Institute Davos, Davos, Switzerland.
Claudia SiverinoAO Research Institute Davos, Davos, Switzerland.
Lena GensAO Research Institute Davos, Davos, Switzerland.ORCID http://orcid.org/0000-0001-8844-9096
Stephan ZeiterAO Research Institute Davos, Davos, Switzerland.ORCID http://orcid.org/0000-0002-8155-4202
Alisa HangartnerAO Research Institute Davos, Davos, Switzerland.
Sandrine HarzéLaboratory of Gene Technology, Department of Biosystems, KU Leuven, Leuven, Belgium.
Eliane VanhoffelenBiomedical MRI, Department of Imaging and Pathology, KU Leuven, Leuven, Belgium.ORCID http://orcid.org/0000-0003-1938-254X
Camille Van LaereLaboratory of Gene Technology, Department of Biosystems, KU Leuven, Leuven, Belgium.
Alison KerremansLaboratory of Gene Technology, Department of Biosystems, KU Leuven, Leuven, Belgium.
Marleen VoetLaboratory of Gene Technology, Department of Biosystems, KU Leuven, Leuven, Belgium.
Maarten BoonLaboratory of Gene Technology, Department of Biosystems, KU Leuven, Leuven, Belgium.ORCID http://orcid.org/0000-0003-3179-0677
Tine Van WinBiomedical MRI, Department of Imaging and Pathology, KU Leuven, Leuven, Belgium.ORCID http://orcid.org/0009-0001-0657-1328
Greetje Vande VeldeBiomedical MRI, Department of Imaging and Pathology, KU Leuven, Leuven, Belgium.ORCID http://orcid.org/0000-0002-5633-3993
Jeroen WagemansLaboratory of Gene Technology, Department of Biosystems, KU Leuven, Leuven, Belgium.ORCID http://orcid.org/0000-0002-2185-5724
Willem-Jan MetsemakersDepartment of Trauma Surgery, University Hospitals Leuven, Leuven, Belgium.ORCID http://orcid.org/0000-0002-4114-9093
Robert Geoffrey RichardsAO Research Institute Davos, Davos, Switzerland.ORCID http://orcid.org/0000-0002-7778-2480
Thomas Fintan Moriarty *AO Research Institute Davos, Davos, Switzerland. fintan.moriarty@aofoundation.org.ORCID http://orcid.org/0000-0003-2307-0397
Rob Lavigne *Laboratory of Gene Technology, Department of Biosystems, KU Leuven, Leuven, Belgium. rob.lavigne@kuleuven.be.ORCID http://orcid.org/0000-0001-7377-1314

Funding

AO Foundation (AO) A118933KU Leuven (Katholieke Universiteit Leuven) C3/23/005
6 · The paper itself

Abstract

The rise of antibiotic resistance, particularly among pathogens such as methicillin-resistant Staphylococcus aureus, necessitates innovative antibacterial strategies. Here we introduce FibriLysins, a class of engineered enzymes combining staphylokinase and endolysin, which dismantle fibrin-encapsulated multicellular staphylococcal communities, including biofilms and staphylococcal abscess communities (SACs). We characterized diverse staphylokinases, developing a library of 27 FibriLysins, with a 78% positive hit rate. The lead variant, FL-028, has significant antibacterial activity against prevalent clinical S. aureus isolates. In vitro, FL-028 reduced bacterial counts in SACs by 3.4 log and in biofilms by 2.3 log. In vivo, FL-028 exhibits superior efficacy in a mouse model of bone fracture-related infection, outperforming vancomycin by 1 log and eliminating SAC presence in tissues. FL-028 shows no adverse effects on bone healing, as confirmed by histological examination, mechanical testing and micro-computed tomography analyses. These preclinical findings highlight the potential of FibriLysins as a robust and safe therapeutic approach against difficult-to-treat staphylococcal infections.

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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.