Atopic dermatitis is a frequent chronic inflammatory skin disease affecting up to 20% of children and 8% of adults in developed countries. The disease is often localized with predilection for the face and limb folds but can be more widespread. AD is a chronic condition with many patterns of natural history the most frequent of which starting during infancy with spontaneous resolution after several years of an evolution characterized by alternance of flares and remissions. Other natural history profiles are also frequent and the disease is prevalent in adults as well, whether as a continuation of pediatric forms or as later onset diseases. Flares and remissions may as well altern in many different ways. AD is often associated with other atopic conditions including asthma, conjunctivitis and rhinitis5. Per se, the disease generates erythematous vesiculous plaques often associated with pruritis1. With time, lesion may become thicker (i.e. lichenified) and pruritus significantly impacts quality of life and sleep quality. The chronic and recurrent evolution is also felt as a burden by many patients and parents.

Taking into account the various signs and symptoms (including itch and sleep disturbance), scores have been developed to properly assess severity and guide treatment, SCORAD being one of them used both in clinical practice and clinical research. Between flares, AD management aims at preventing recurrence by avoiding triggering factors and restoring skin barrier through daily application of emollients. During flares, topical steroids are more often used than calcineurin inhibitors mostly dedicated to sensitive areas (face, folds). More severe or resistant cases deserve phototherapy or systemic immunomodulatory treatments with many new drug candidates under clinical development. Back to topical treatments, many failures are due to improper usage of topical steroids because of corticophobia. As for calcineurin inhibitors, irritation is the main limiting factor10,11. This is where important room remains for new topical treatments with good safety and tolerance profiles leading to proper usage and good observance over time and avoiding as much as possible steroid application. Crisaborole has recently been authorized in the US and JAK inhibitors are currently under investigation which illustrates the actual need. AD pathophysiology is complex and its apprehension evolves over time. Current vision associates genetic background and environmental triggering factors. Three mains factors interact to generate AD namely 1) skin barrier defect, 2) skin inflammation driven by T lymphocytes and 3) dysbiosis through the decrease of skin microbiome diversity and staphylococcus proliferation. All three are deeply interlinked. Focusing on the latter, evidence is available that microbiome is disturbed during AD. Whether this dysbiosis is a cause or a consequence remains sometimes debated, but growing evidence suggests a causative relationship especially through S. aureus proliferation, at least as an aggravative factor. Indeed S. aureus is way more frequent on AD skin with good correlation with AD severity. Some of S aureus virulence factors (superantigens, enterotoxins, alphatoxins, proteases activators production) provide a good rational for it from a mechanistic standpoint. The decrease of the microbiome diversity, the role of which is to avoid pathogens proliferation, may play a role in S. aureus proliferation on AD skin, together with skin barrier and immune defect.

Therefore, making available well tolerated and easy to use topical products avoiding S. aureus proliferation and dysbiosis fully makes sense whether as standalone or companion products both in flares management and prevention of recurrences.

In this study, the sponsor will test a well tolerated topical product including a phage derived recombinant endolysine (Staphefekt®) with a capacity to specifically destroy S aureus regardless of its methicillin sensitivity. The product will be tested alone, in children and adults with acute mild to moderate AD i.e as an alternative to alternative treatments, over 6 weeks.