Abstract
Wound dressings with silver have been shown to be cytotoxic in vitro. However, the extrapolation of this cytotoxicity to clinical settings is unclear. We applied dressings with various forms of silver on porcine skin ex vivo and investigated silver penetration and DNA damage. We assessed antimicrobial efficacy, cytotoxicity to skin cells, and immune response induced by the dressings. All dressings elevated the DNA damage marker γ-H2AX and the expression of stress-related genes in explanted skin relative to control. This corresponded with the amount of silver in the skin. The dressings reduced viability, induced oxidative stress and DNA damage in skin cells, and induced the production of pro-inflammatory IL-6 by monocytes. The oxidative burst and viability of activated neutrophils decreased. The amount of silver released into the culture medium varied among the dressings and correlated with in vitro toxicity. However, antimicrobial efficiencies did not correlate strongly with the amount of silver released from the dressings. Antimicrobial efficiency and toxicity are driven by the form of silver and the construction of dressings and not only by the silver concentration. The damaging effects of silver dressings in ex vivo skin highlight the importance of thorough in vivo investigation of silver dressing toxicity.
Highlights
Wound dressings with silver have been shown to be cytotoxic in vitro
We evaluated four dressings used in the treatment of chronic non-healing or hard-to-heal wounds
We investigated the physicochemical properties of silver contained in wound dressings and the induction of selected toxic and antimicrobial processes in vitro and ex vivo by these dressings
Summary
Wound dressings with silver have been shown to be cytotoxic in vitro. the extrapolation of this cytotoxicity to clinical settings is unclear. We applied dressings with various forms of silver on porcine skin ex vivo and investigated silver penetration and DNA damage. All dressings elevated the DNA damage marker γ-H2AX and the expression of stress-related genes in explanted skin relative to control. This corresponded with the amount of silver in the skin. The dressings reduced viability, induced oxidative stress and DNA damage in skin cells, and induced the production of proinflammatory IL-6 by monocytes. Due to silver’s narrow therapeutic window, eukaryotic cells can be damaged by silver in the wound together with the pathogens by both direct contact with Ag+ or Ag0 nanoparticles and indirectly by ROS, which may result in suboptimal healing
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