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Updated: May 24, 2026
A Delayed Inoculation Model of Chronic Pseudomonas aeruginosa Wound Infection
Published on: February 20, 2020
Impact of Pseudomonas aeruginosa quorum sensing on cellular wound healing responses in vitro
Jasper N Jacobsen1, Anders S Andersen, Karen A Krogfelt
1Department of Microbiological Surveillance and Research, Statens Serum Institut, Copenhagen S, Denmark.
Abstract:
The virulent capacity of Pseudomonas aeruginosa can largely be ascribed to quorum sensing, i.e. the ability to evade host defence by a coordinated production and secretion of virulence factors. When P. aeruginosa is harboured in chronic wounds, a non-healing condition is often observed. In this study, we examined the in vitro cellular responses of the major cell types of re-epithelialization to supernatants of P. aeruginosa wild-type or an isogenic mutant not expressing quorum sensing-regulated virulence genes. We observed impairment of cell migration in keratinocytes (p = 0.009) and fibroblasts (p = 0.043) when supplementing medium with 20% P. aeruginosa culture supernatants. Cell proliferation was not significantly reduced, except for keratinocytes (p = 0.040). Data show compliance with in vivo observations of proliferating, non-motile epithelial cell behaviour in bacterially contaminated chronic wounds. Our findings suggest that quorum sensing may serve as an interesting target for controlling P. aeruginosa virulence in modern wound care.
Insights
Pseudomonas aeruginosa quorum sensing impairs keratinocyte and fibroblast migration, crucial for chronic wound healing. Targeting this bacterial communication could improve wound care strategies.
Area of Science:
- Microbiology
- Cell Biology
- Wound Healing Research
Background:
- Pseudomonas aeruginosa virulence is linked to quorum sensing, enabling coordinated virulence factor production.
- Chronic wounds often harbor P. aeruginosa, leading to non-healing conditions.
- Quorum sensing regulates bacterial communication and virulence factor expression.
Purpose of the Study:
- To investigate the in vitro effects of P. aeruginosa quorum sensing on key cell types involved in wound re-epithelialization.
- To compare cellular responses to wild-type P. aeruginosa with a mutant lacking quorum sensing-regulated virulence genes.
Main Methods:
- Exposure of keratinocytes and fibroblasts to supernatants from P. aeruginosa wild-type and quorum sensing-deficient mutant strains.
- Assessment of cell migration and proliferation rates in response to bacterial supernatants.
- In vitro cell culture models simulating wound re-epithelialization processes.
Main Results:
- P. aeruginosa supernatants significantly impaired keratinocyte and fibroblast cell migration.
- Cell proliferation was generally unaffected, with a minor reduction observed in keratinocytes.
- Observed cellular behaviors align with in vivo findings in chronic wounds.
Conclusions:
- Quorum sensing-mediated virulence factors from P. aeruginosa negatively impact critical cellular processes for wound repair.
- Inhibition of P. aeruginosa quorum sensing presents a potential therapeutic target for managing chronic wound infections.
- Understanding bacterial communication is vital for developing advanced wound care interventions.
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