A dysfunctional epidermal barrier, which may be associated with mutations in the filaggrin gene in genetically predisposed individuals or harmful effects of environmental agents and allergens, contributes to the development of atopic dermatitis (AD) due to an interplay between the epithelial barrier, immune defence and the cutaneous microbiome. The skin of patients with AD is frequently over‐colonized by biofilm‐growing Staphylococcus aureus, especially during flares, causing dysbiosis of the cutaneous microbiota and a decrease in bacterial diversity that inversely correlates with AD severity. Specific changes in the skin microbiome can be present before clinical AD onset in infancy. Additionally, local skin anatomy, lipid content, pH, water activity and sebum secretion differ between children and adults and generally correlate with the predominant microbiota. Considering the importance of S. aureus in AD, treatments aimed at reducing over‐colonization to rebalance microbial diversity may help manage AD and reduce flares. Anti‐staphylococcal interventions in AD will contribute to a decrease in S. aureus superantigens and proteases that cause damage and inflammation of the skin barrier while concomitantly increasing the proportion of commensal bacteria that secrete antimicrobial molecules that protect healthy skin from invading pathogens. This review summarizes the latest data on targeting skin microbiome dysbiosis and S. aureus over‐colonization to treat AD in adults and children. Indirect AD therapies, including emollients ‘plus’, anti‐inflammatory topicals and monoclonal antibodies, may have an impact on S. aureus and help control bacterial diversity. Direct therapies, including antibacterial treatments (antiseptics/topical or systemic antibiotics), and innovative treatments specifically targeting S. aureus (e.g. anti‐S. aureus endolysin, and autologous bacteriotherapy), may be effective alternatives to mitigate against an increase in microbial resistance and allow a proportionate increase in the commensal microbiota.

Objective To decode the feeling of skin tightness after application of a cosmetic product and how to soothe this discomfort. To pursue this aim, we considered the ingredient's effect on stratum corneum (SC) biomechanics to differentiate between consumers prone to tightness from those that are not and correlate these effects with mechanoreceptor activation. Methods In vivo clinical trials were used to assess the tightness perception dichotomy between groups of Caucasian women; in vitro experiments were used to measure the mechanical stresses induced in the SC after cleanser and moisturizer application; and in silico simulations were used to illustrate how the measured mechanical stresses in the SC result in the development of strains at the depth of cutaneous mechanoreceptors, triggering tightness perceptual responses. Results Before any cream application, women prone to tightness tend to have a more rigid SC than their less sensitive counterparts, however cleanser application increases SC stiffness in all women. Surprisingly, no correlation was found between tightness perception and hydration measurements by the Corneometer or barrier function, as evaluated by transepidermal water loss. Self‐declared tightness and dryness scores were strongly associated with a self‐described sensitive skin. After application of the optimized moisturizing formula, Osmoskin® containing natural waxes with good filming properties, consumers report a strong decrease in tightness and dryness perception. These results match with laboratory experiments where the cleanser was shown to increase SC drying stresses by 34%, while subsequent application of Osmoskin® decreased stresses by 48%. Finite element modelling, using experimental results as input, elucidates the differences in perception between the two groups of women. It makes clear that Osmoskin® changes the mechanical status of the SC, producing strains in underlying epidermis that activates multiple cutaneous mechano‐receptors at a level correlated with the self‐perceived comfort. Conclusion Integration of the in vivo, in vitro and in silico approaches provides a novel framework for fully understanding how skin tightness sensations form and propagate, and how these sensations can be alleviated through the design of an optimized moisturizer.

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