Pseudomonas aeruginosa biofilm hampers murine central wound healing by suppression of vascular epithelial growth factor. Issue 1 (27th November 2017)

• Record Type: Journal Article
• Authors: Trøstrup, Hannah; Lerche, Christian J.; Christophersen, Lars J.; Thomsen, Kim; Jensen, Peter Ø.; Hougen, Hans Petter; Høiby, Niels; Moser, Claus
• Is Part Of: International wound journal. Volume 15:Issue 1(2018)
• Page Start: 123
• Page End: 132
• Publication Date: 2017-11-27
• Subjects: Chronic wounds -- Pseudomonas aeruginosa biofilm infection -- S100A8/A9 -- Vascular endothelial growth factor -- Wound necrosis; Wounds and injuries -- Treatment -- Periodicals; Wounds and injuries -- Periodicals; Wound healing -- Periodicals; 617.1005
• DOI: 10.1111/iwj.12846
• Languages: English
• ISSNs: 1742-4801

Abstract

Abstract: Biofilm‐infected wounds are clinically challenging. Vascular endothelial growth factor and host defence S100A8/A9 are crucial for wound healing but may be suppressed by biofilms. The natural course of Pseudomonas aeruginosa biofilm infection was compared in central and peripheral zones of burn‐wounded, infection‐susceptible BALB/c mice, which display delayed wound closure compared to C3H/HeN mice. Wounds were evaluated histopathologically 4, 7 or 10 days post‐infection. Photoplanimetry evaluated necrotic areas. P. aeruginosa biofilm suppressed vascular endothelial growth factor levels centrally in BALB/c wounds but increased peripheral levels 4–7 days post‐infection. Central zones of the burn wound displayed lower levels of central vascular endothelial growth factor as observed 4 and 7 days post‐infection in BALB/c mice compared to their C3H/HeN counterparts. Biofilm suppressed early, centrally located S100A8/A9 in BALB/c and centrally and peripherally later on in C3H/HeN wounds as compared to uninfected mice. Peripheral polymorphonuclear‐dominated inflammation and larger necrosis were observed in BALB/c wounds. In conclusion, P. aeruginosa biofilm modulates wounds by suppressing central, but inducing peripheral, vascular endothelial growth factor levels and reducing host response in wounds of BALB/c mice. This suppression is detrimental to the resolution of biofilm‐infected necrosis.