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Updated: Sep 7, 2025

A Delayed Inoculation Model of Chronic Pseudomonas aeruginosa Wound Infection
Published on: February 20, 2020
Filamentous bacteriophage delays healing of Pseudomonas-infected wounds
Michelle S Bach1, Christiaan R de Vries2, Arya Khosravi2
1Division of Infectious Diseases and Geographic Medicine, Department of Medicine, Stanford University, Stanford, CA 94305, USA; Stanford Immunology, Stanford University, Stanford, CA 94305, USA.
Abstract:
Chronic wounds infected by Pseudomonas aeruginosa (Pa) are characterized by disease progression and increased mortality. We reveal Pf, a bacteriophage produced by Pa that delays healing of chronically infected wounds in human subjects and animal models of disease. Interestingly, impairment of wound closure by Pf is independent of its effects on Pa pathogenesis. Rather, Pf impedes keratinocyte migration, which is essential for wound healing, through direct inhibition of CXCL1 signaling. In support of these findings, a prospective cohort study of 36 human patients with chronic Pa wound infections reveals that wounds infected with Pf-positive strains of Pa are more likely to progress in size compared with wounds infected with Pf-negative strains. Together, these data implicate Pf phage in the delayed wound healing associated with Pa infection through direct manipulation of mammalian cells. These findings suggest Pf may have potential as a biomarker and therapeutic target in chronic wounds.
Insights
A bacteriophage called Pf, produced by Pseudomonas aeruginosa (Pa), delays chronic wound healing by directly inhibiting keratinocyte migration. This discovery suggests Pf could be a biomarker and therapeutic target for persistent wound infections.
Area of Science:
- Microbiology
- Wound Healing Research
- Bacteriophage Therapy
Background:
- Chronic wounds infected with Pseudomonas aeruginosa (Pa) often show disease progression and higher mortality.
- Bacteriophages, viruses that infect bacteria, are being investigated for their role in infection dynamics.
Purpose of the Study:
- To investigate the role of a specific bacteriophage, Pf, produced by Pa, in the delayed healing of chronic wounds.
- To elucidate the mechanism by which Pf affects wound closure, independent of its bacterial pathogenesis.
Main Methods:
- Analysis of Pf's effect on wound closure in human and animal models.
- Investigation of Pf's impact on keratinocyte migration and CXCL1 signaling.
- A prospective cohort study of 36 human patients with chronic Pa wound infections.
Main Results:
- Pf significantly delays chronic wound healing.
- Pf impedes keratinocyte migration by directly inhibiting CXCL1 signaling, independent of Pa pathogenesis.
- Human patients with Pf-positive Pa strains had wounds that progressed more in size compared to those with Pf-negative strains.
Conclusions:
- The Pf bacteriophage directly manipulates mammalian cells, specifically inhibiting keratinocyte migration via CXCL1 signaling, leading to delayed wound healing.
- Pf is implicated as a key factor in the delayed healing of chronic wounds infected by Pa.
- Pf shows potential as a biomarker for wound progression and a therapeutic target for chronic wound infections.
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