THE WAR UNDER THE SKIN - BIOFILM AND INFLAMMATION IN CHRONIC WOUNDS

The skin, the largest organ in the body, protects against external stimuli and microorganisms. A balanced skin microbiota, including both commensal and pathogenic microorganisms, is essential for skin health. Disruptions in this balance can lead to infections and inflammation, which are key factors in delayed wound healing. Biofilm formation further complicates the process. In chronic wounds, healing is often impaired during the inflammatory phase due to persistent activation of the immune response. This leads to increased immune cell activation, along with heightened activity of matrix metalloproteinases (MMPs), collagenase, and elastase, while tissue inhibitors of matrix metalloproteinases (TIMPs) decrease. Host factors such as wound depth, duration, local hypoxia, and immune responses contribute to healing delays. Microbial factors, including bacterial diversity, microbial load, and pathogenicity, also play a significant role. Biofilms are more resistant to antimicrobial therapy than free-floating bacteria. Its formation in chronic wounds triggers sustained inflammation, marked by elevated inflammatory mediators like IL-6, IL-10, IL-17A, and TNF-α. Biofilms not only prolong inflammation but also cause oxidative stress and protease-mediated degradation of essential receptors and cytokines, accelerating wound bed senescence. The presence and persistence of biofilm in chronic wounds affect the host’s immune response. Understanding this relationship offers more opportunities for successful treatment.