Atopic dermatitis (AD) is a chronic inflammatory skin disease affecting up to 20% of children and 10% of adults worldwide. It is characterized by itching, inflammatory lesions, and dry skin. A key factor in this condition is excessive colonization of the skin by Staphylococcus aureus<\/em>, which disrupts the skin barrier and exacerbates inflammation. This colonization is frequently observed in lesions and even on unaffected skin areas. At the same time, skin microbial diversity is often reduced, limiting the presence of beneficial commensal microbes (1\u20135).<\/p>\n AD results from a complex interaction between genetic predispositions, alterations of the skin barrier, dysbiosis of the skin microbiome, and environmental factors (3,6). Barrier dysfunction is linked to genetic mutations, notably in the FLG<\/strong> gene encoding filaggrin, which is essential for skin hydration and protection. This mutation, in addition to downregulating certain structural proteins, promotes antigen sensitization (6). AD is also associated with an imbalanced immune response dominated by Th2 and Th17 cytokines (3). Epigenetics and the exposome, including the influence of environmental pollutants and oxidative stress, play a crucial role in the disease\u2019s pathogenesis. The \u201catopic march,\u201d a phenomenon encompassing the transition from atopic dermatitis to other allergic conditions such as asthma and rhinitis, illustrates how atopic symptoms can evolve from a very young age (1).<\/p>\n Beyond Staphylococcus aureus<\/em>, other microorganisms influence the course of atopic dermatitis. Staphylococcus epidermidis<\/em> usually plays a protective role by limiting the proliferation of S. aureus<\/em> through the production of antimicrobial molecules; however, its presence is often reduced in dysbiosis. Byrd et al. showed that milder AD flares were associated with higher levels of S. epidermidis<\/em>, whereas more severe flares correlated with S. aureus<\/em>. Conversely, certain yeasts of the genus Malassezia<\/em> may contribute to worsening symptoms, particularly during inflammatory flares (6,7,8).<\/p>\n Management of AD relies on conventional therapies such as topical corticosteroids and antibiotics, as well as practices like diluted bleach baths (9). Innovative approaches include autologous microbiotherapy, the use of probiotics and prebiotics to rebalance the skin microbiome, and JAK inhibitors to reduce inflammation (6). A better understanding of these factors will enable the development of personalized treatments aimed at improving patients\u2019 quality of life. Microbiome-friendly treatments may also be very beneficial for atopic skin. Strategies that reduce S. aureus<\/em> colonization while promoting the expansion of S. epidermidis<\/em> or other beneficial commensal bacteria also represent a promising avenue for new treatments.<\/p>\n At the request of a client developing a cream for atopic-prone skin, BYOME LABS designed a bespoke protocol to evaluate, through in vitro tests, its impact on Staphylococcus aureus<\/em> in both planktonic and biofilm forms. Our experts selected the relevant strains based on the scientific literature and data from other microbiome study techniques (NGS sequencing). After an initial phase of planktonic testing, the study focused on the cream\u2019s preventive effect on biofilm formation. Result: the product did not show a bactericidal effect, but it demonstrated an ability to limit biofilm formation, making S. aureus<\/em> colonization more transient.<\/p>\n At BYOME LABS, our teams tailor their know-how to your products and objectives and support you throughout the entire process.<\/p>\n <\/p>\nCauses<\/h1>\n
What about other microorganisms?<\/h1>\n
Treatments<\/h1>\n
BYOME LABS case study<\/h1>\n