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Peer-reviewedCC BY-NC-ND 4.0NPJ Biofilms and Microbiomes

Long-term spatiotemporal biological and mechanobiological dynamics of Staphylococcus aureus biofilms

  • Silvia Cometta1,2,3
  • Maria de los Reyes Becerra Perez2
  • Inbar Shmuely4,5
  • Flavia Medeiros Savi1,2,3
  • Liraz Chai1,4,5
  • Dietmar W. Hutmacher1,2,3,6
6 affiliations
  1. 1Max Planck Queensland Centre, Queensland University of Technology, Brisbane, QLD Australia
  2. 2Faculty of Engineering, School of Mechanical, Medical and Process Engineering, Queensland University of Technology, Brisbane, QLD Australia
  3. 3Australian Research Council Training Centre for Multiscale 3D Imaging, Modelling and Manufacturing (M3D Innovation), Queensland University of Technology, Brisbane, QLD Australia
  4. 4Institute of Chemistry, The Hebrew University of Jerusalem, Jerusalem, Israel
  5. 5The Center for Nanoscience and Nanotechnology, The Hebrew University of Jerusalem, Jerusalem, Israel
  6. 6Australian Research Council Training Centre for Cell and Tissue Engineering Technologies, Queensland University of Technology, Brisbane, QLD Australia
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Abstract

In the context of implanted medical devices, biofilm formation transforms otherwise inert biomaterials into persistent sources of infection that are highly resistant to antimicrobial therapy and immune clearance. This persistent problem demands a critical re-examination of how biofilms are conceptualized, studied, and modeled. Using tissue-mimicking gelatin methacryloyl hydrogels, we show that Staphylococcus aureus spatiotemporal biofilm dynamics are strongly regulated by matrix mechanics and nutrient availability. Nutrient-rich conditions promote hyperproliferative, eDNA-rich microcolonies that actively degrade polymer networks, whereas serum-supplemented conditions produce compact aggregates enriched with vesicle-like structures and serum-derived matrix components. Notably, 3D confinement revealed a previously unrecognized ‘budding’ dispersal mechanism unique to embedded biofilms. Integrating 3D-printed polycaprolactone implants shows that while implant surfaces promote bacterial adhesion, the surrounding microenvironment exerts primary regulatory control. Longitudinal tracking over 3 weeks recapitulates key biofilm hallmarks and challenges surface-centric paradigms of implant infections, providing a framework for dissecting infection mechanisms and guiding therapeutic strategies.

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Cite

BibTeXRIS
BibTeX
@article{cometta2026longterm,
  title = {{Long-term spatiotemporal biological and mechanobiological dynamics of Staphylococcus aureus biofilms}},
  author = {Silvia Cometta and Maria de los Reyes Becerra Perez and Inbar Shmuely and Flavia Medeiros Savi and Liraz Chai and Dietmar W. Hutmacher},
  journal = {NPJ Biofilms and Microbiomes},
  year = {2026},
  month = jul,
  doi = {10.1038/s41522-026-01097-2},
  url = {https://doi.org/10.1038/s41522-026-01097-2},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Long-term spatiotemporal biological and mechanobiological dynamics of Staphylococcus aureus biofilms
AU  - Silvia Cometta
AU  - Maria de los Reyes Becerra Perez
AU  - Inbar Shmuely
AU  - Flavia Medeiros Savi
AU  - Liraz Chai
AU  - Dietmar W. Hutmacher
PY  - 2026
DA  - 2026/07/13
JO  - NPJ Biofilms and Microbiomes
DO  - 10.1038/s41522-026-01097-2
UR  - https://doi.org/10.1038/s41522-026-01097-2
AB  - In the context of implanted medical devices, biofilm formation transforms otherwise inert biomaterials into persistent sources of infection that are highly resistant to antimicrobial therapy and immune clearance. This persistent problem demands a critical re-examination of how biofilms are conceptualized, studied, and modeled. Using tissue-mimicking gelatin methacryloyl hydrogels, we show that Staphylococcus aureus spatiotemporal biofilm dynamics are strongly regulated by matrix mechanics and nutrient availability. Nutrient-rich conditions promote hyperproliferative, eDNA-rich microcolonies that actively degrade polymer networks, whereas serum-supplemented conditions produce compact aggregates enriched with vesicle-like structures and serum-derived matrix components. Notably, 3D confinement revealed a previously unrecognized ‘budding’ dispersal mechanism unique to embedded biofilms. Integrating 3D-printed polycaprolactone implants shows that while implant surfaces promote bacterial adhesion, the surrounding microenvironment exerts primary regulatory control. Longitudinal tracking over 3 weeks recapitulates key biofilm hallmarks and challenges surface-centric paradigms of implant infections, providing a framework for dissecting infection mechanisms and guiding therapeutic strategies.
SN  - 2055-5008
ER  -