Charachterization of skin microbiome in 16 individuals affected by Epidermolysis bullosa
Epidermolysis bullosa (EB) is a heterogeneous group of bullous disorders characterized by detachment of the epithelium following minimal mechanical trauma. The phenotypic spectrum is broad, with persistent blistering, inflammation, delayed re-epithelialization, abnormal wound healing and frequent infection leading to disability and, in the most severe cases, death. The human skin microbiome has adapted to produce molecules that inhibit the colonization of pathogenic microorganisms. In EB patients, the skin barrier is broken, and the balance between commensal and pathogenic microorganisms is altered. Understanding shifts in the microbial communities of EB patients may lead to new therapeutic targets to improve management. We used whole-genome sequencing to investigate and characterize shifts from a healthy to an EB-associated skin microbiome. In particular, we sampled skin from blisters, healthy skin surrounding blisters at the time of blister formation and after 48 hours, from dry skin and feet of healthy controls and people with EB. The foot skin microbiota of people affected by EB showed a decreased relative abundance of Actinomycetales, which produce secondary metabolites with antibiotic, antifungal and anticancer properties. In addition, we observed in dry skin of people affected by EB a striking reduction of the skin commensal Malasezia globosa, known to limit and attenuate Staphylococcus aureus biofilm formation, protecting the host from infection. Importantly, we found that this fungal dysbiosis is associated with an increased relative abundance of S. aureus in EB patients on blisters and the surrounding area during the wound healing process. These spatiotemporal shifts may be involved in the pathophysiology of atypical wound healing, increased risk of wound infection and skin cancer. Further understanding of the reported dysbiosis may present opportunities for improved interventions, leading to improved quality of life.