Abstract
Normal wound healing occurs in three phases—the inflammatory, the proliferative, and the remodeling phase. Chronic wounds are, for unknown reasons, arrested in the inflammatory phase. Bacterial biofilms may cause chronicity by arresting healing in the inflammatory state by mechanisms not fully understood. Pseudomonas aeruginosa, a common wound pathogen with remarkable abilities in avoiding host defense and developing microbial resistance by biofilm formation, is detrimental to wound healing in clinical studies. The host response towards P. aeruginosa biofilm-infection in chronic wounds and impact on wound healing is discussed and compared to our own results in a chronic murine wound model. The impact of P. aeruginosa biofilms can be described by determining alterations in the inflammatory response, growth factor profile, and count of leukocytes in blood. P. aeruginosa biofilms are capable of reducing the host response to the infection, despite a continuously sustained inflammatory reaction and resulting local tissue damage. A recent observation of in vivo synergism between immunomodulatory and antimicrobial S100A8/A9 and ciprofloxacin suggests its possible future therapeutic potential.
Highlights
Normal wound healing is a complicated, tightly regulated process in which a proliferative phase succeeds inflammation
Chronic wounds are arrested in the inflammatory phase of wound healing for reasons that are unknown
P. aeruginosa biofilm affects wound healing negatively via alterations in host defense mechanisms; polymorphonuclear leucocytes (PMNs) are initially recruited to the site of infection
Summary
Normal wound healing is a complicated, tightly regulated process in which a proliferative phase succeeds inflammation. Superficial venous insufficiency can be managed by surgical intervention or split skin transplant in the case of non-healing wounds, this is often challenged by P. aeruginosa biofilm infection [9]. Similar results may be obtained by the wound application of autologous patches, constituting of leucocytes, thrombocytes, and fibrin generated from the patient’s own blood by special centrifugation [11] Such application was shown to improve the healing of hard-to-heal diabetic ulcers as compared to the standard of care [12], and gives hope for new treatment approaches. Observations in mouse models will be considered for this review With this background, implications for clinical wound healing are discussed and, whether immunomodulatory topical treatment with the antimicrobial peptide, S100A8/A9, could be an adjuvant therapy strategy in chronic biofilm infections is discussed. Host/Pathogen Interactions in Chronic Wounds and Implications for Wound Healing
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