Chronic Pseudomonas aeruginosa biofilm infection impairs murine S100A8/A9 and neutrophil effector cytokines—implications for delayed wound closure?

Research output: Contribution to journalJournal articleResearchpeer-review

The impact of Pseudomonas aeruginosa biofilm infections in chronic wounds and clinical implication for healing is receiving increased attention. However, the pathophysiology of host/pathogen interplay is not fully understood. By further revealing the mechanisms, necessary new treatment strategies may be identified. Since the background for chronic wounds is diverse, representative animal models are important. We assessed host response and spontaneous wound closure in the relatively resistant C3H/HeN and the susceptible BALB/c mouse strain. Full-thickness burn wounds were inflicted in 108 mice. P. aeruginosa biofilm (106 colony forming units) was injected subcutaneously in 72 mice, euthanized day 4, 7 or 10 days postinfection. Wounds were analysed for neutrophil host response markers: S100A8/A9, keratinocyte-derived chemokine and Granulocyte-Colony Stimulating Factor. Total peripheral blood leukocyte and polymorphonuclear count were assessed in parallel. Histopathology evaluated wound inflammatory burden. Photoplanimetry described macroscopical wound closure. Stable chronic wound infection was established in all challenged mice. P. aeruginosa biofilm suppressed neutrophil host response in wounds. C3H/HeN mice achieved earlier systemic inflammatory control and healed faster than BALB/c mice. P. aeruginosa biofilms perturbs host defense thereby inducing a steady-state of chronic infection which may impair wound healing. These results indicate therapeutic options for immune modulation of biofilm-infected wounds.

Original languageEnglish
Article numberftx068
JournalPathogens and Disease
Issue number7
Number of pages10
Publication statusPublished - Oct 2017

Bibliographical note


ID: 179847641