INTRODUCTION
Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disorder that typically begins in infancy or early childhood, affecting up to 20% of children and 10% of adults globally, with significant variability in clinical presentation and disease severity.1 The disease is characterized by a cycle of interdependent pathological presentations, inflammation, skin dysbiosis predominantly involving Staphylococcus aureus (S. aureus) and subsequent infection, intense pruritus, and xerosis.1,2 These features, termed the "four demons," perpetuate and exacerbate one another along an AD Continuum, complicating effective disease management and profoundly affecting quality of life.2-4
The pathogenesis of AD is multifactorial, driven by complex interactions among various SAIGE triggers: S. aureus colonization/infection, immune dysregulation, genetic predisposition, and environmental influences.5,6 Evidence suggests that these SAIGE factors contribute to both disease exacerbation and onset, with S. aureus colonization preceding clinical manifestations and driving inflammation as well as directly inducing pruritus through neuroimmune interactions.7-9
Despite advances in AD therapies, current treatments do not comprehensively address the entire AD Continuum and the underlying SAIGE triggers.10-12 Limitations in management strategies, combined with the complexity of AD and its
