| Summary: | (1) Background alteration of the skin microbiota, dysbiosis, causes skin barrier impairment resulting in disease development. <i>Staphylococcus aureus</i>, the main pathogen associated with dysbiosis, secretes several virulence factors, including α-toxin that damages tight junctions and compromises the integrity of the skin barrier. The use of members of the resident microbiota to restore the skin barrier, bacteriotherapy, represents a safe treatment for skin conditions among innovative options. The aim of this study is the evaluation of a wall fragment derived from a patented strain of <i>Cutibacterium acnes</i> DSM28251 (c40) alone and conjugated to a mucopolysaccharide carrier (HAc40) in counteracting <i>S. aureus</i> pathogenic action on two tight junction proteins (Claudin-1 and ZO-1) in an ex vivo porcine skin infection model. Methods: skin biopsies were infected with live <i>S. aureus</i> strains ATCC29213 and DSM20491. Tissue was pre-incubated or co-incubated with c40 and HAc40. (3) Results: c40 and HAc40 prevent and counteract Claudin-1 and Zo-1 damage (4) Conclusions: c40 and the functional ingredient HAc40 represent a potential non-pharmacological treatment of skin diseases associated with cutaneous dysbiosis of <i>S. aureus</i>. These findings offer numerous avenues for new research.
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