INTRODUCTION
Atopic dermatitis (AD) affects 20% of infants and adolescents and up to 3% of adults worldwide1,2 and its incidence is increasing globally.3 AD causes erythema, constant intense itching,4 and psychological distress5 which negatively impacts quality of life (QoL) more than other chronic conditions such as heart disease or diabetes.6 In children, it has the second highest impact on QoL.7
AD is a chronic inflammatory skin condition associated with epidermal barrier dysfunction, abnormal immune response, and skin microbiome imbalance.8 These three factors are interdependent thus enabling AD symptoms to be managed from multiple angles. Skin microbiome dysbiosis is often characterized by low skin microbial diversity compared to healthy skin and an over-colonization of S. aureus.9 S. aureus levels are associated with AD disease severity, flare frequency and symptoms that directly impact QoL.10-12 Its toxins stimulate proinflammatory cytokine and chemokine production causing itching, burning sensations, and pain,13,14 and create a vicious itch-scratch cycle.15-17
During AD flares, treatment aims to reduce inflammation and itching, rebuild the epidermal barrier, and prevent secondary infections.18 Appropriate moisturizers and cleansers are cornerstones of AD management to address skin barrier dysfunction.19 Topical corticosteroids (TCS) are first-line treatment for flares since they effectively reduce inflammation.20 However, their use is limited to avoid developing skin atrophy in sensitive skin areas.21 Furthermore, patients express concerns (corticophobia) which can impactTCS use, adherence to treatment and overall effectiveness.22 Secondary infection, particularly by S. aureus, can be treated with broad spectrum or anti-staphylococcal antibiotics20 but these can damage the beneficial skin microbiota and potentially lead to antibiotic resistance.23 Considering the mounting evidence pointing towards the major negative role of S. aureus in AD and the beneficial role of the skin microbiome for skin homeostasis, a treatment exclusively targeting S. aureus offers many advantages.24
Many microbial ecosystems, including the skin microbiome, harbor viruses called bacteriophages that only infect bacteria.25 Bacteriophages are specific for their target bacteria, and at the end of their lytic cycle induce the production of enzymes, called endolysins, which degrade the peptidoglycan of the bacterial cell wall from within, causing cell lysis and progeny virion release. Since Gram-positive bacteria, such as S. aureus,
AD is a chronic inflammatory skin condition associated with epidermal barrier dysfunction, abnormal immune response, and skin microbiome imbalance.8 These three factors are interdependent thus enabling AD symptoms to be managed from multiple angles. Skin microbiome dysbiosis is often characterized by low skin microbial diversity compared to healthy skin and an over-colonization of S. aureus.9 S. aureus levels are associated with AD disease severity, flare frequency and symptoms that directly impact QoL.10-12 Its toxins stimulate proinflammatory cytokine and chemokine production causing itching, burning sensations, and pain,13,14 and create a vicious itch-scratch cycle.15-17
During AD flares, treatment aims to reduce inflammation and itching, rebuild the epidermal barrier, and prevent secondary infections.18 Appropriate moisturizers and cleansers are cornerstones of AD management to address skin barrier dysfunction.19 Topical corticosteroids (TCS) are first-line treatment for flares since they effectively reduce inflammation.20 However, their use is limited to avoid developing skin atrophy in sensitive skin areas.21 Furthermore, patients express concerns (corticophobia) which can impactTCS use, adherence to treatment and overall effectiveness.22 Secondary infection, particularly by S. aureus, can be treated with broad spectrum or anti-staphylococcal antibiotics20 but these can damage the beneficial skin microbiota and potentially lead to antibiotic resistance.23 Considering the mounting evidence pointing towards the major negative role of S. aureus in AD and the beneficial role of the skin microbiome for skin homeostasis, a treatment exclusively targeting S. aureus offers many advantages.24
Many microbial ecosystems, including the skin microbiome, harbor viruses called bacteriophages that only infect bacteria.25 Bacteriophages are specific for their target bacteria, and at the end of their lytic cycle induce the production of enzymes, called endolysins, which degrade the peptidoglycan of the bacterial cell wall from within, causing cell lysis and progeny virion release. Since Gram-positive bacteria, such as S. aureus,
