Effect of a newly developed skin protecting ingredient, acting on skin barrier function and microbiota equilibrium, thus favoring the balance and comfort of reactive skin

  • August 20, 2018
  • 3 mins of read time

Effect of a newly developed skin protecting ingredient, acting on skin barrier function and microbiota equilibrium, thus favoring the balance and comfort of reactive skin

Catherine Kern, Elsa Hernandez, Christian Gombert, Sandy Dumont
2018, 30th IFSCC congress

Human skin is naturally covered with a population of microorganisms, specialized or opportunist, so called skin microbiota. Commensal microbiota contributes to skin defenses and is essential to maintain healthy skin. For example, Staphylococcus epidermidis is the most common bacteria of the cutaneous microbiota. Skin epidermis permits growth of S. epidermidis which itself contributes to protection against pathogens. But this symbiosis is continuously threatened by physical/chemical aggressions, and this imbalance could be beneficial to opportunistic bacteria. Staphylococcus aureus is a leading human pathogen which can cause diseases ranging from minor skin infections to invasive and life-threatening diseases. Generally, dysbiosis between microbiota and skin leads to activation of immune defenses, inflammation and dysfunction of the skin barrier function, and thus to the development of skin disorders, such as dryness, inflammation or sensitivity. Our aim was to investigate the effect of ArL, a newly-developed natural ingredient, on skin protection and comfort of reactive skins, by acting on microbiota equilibrium and skin barrier function.

First, the efficacy of ArL on the skin barrier function was evaluated on a new model of human reconstructed epidermis colonized with S. epidermidis and S. aureus. Growth of both bacteria was measured and the functional impact on the skin barrier as well. ArL was able to limit S. aureus biofilm formation, without impacting its viability nor that of S. epidermidis, probably by promoting mineral charge in favor of S. epidermidis. ArL was able to reinforce skin barrier function by protecting skin integrity, limiting biotin penetration and increasing epidermis and stratum corneum cohesion. The effect of ArL on microbiota balance was further analysed by assessing its protective effect in a model of inflammation resulting from perturbation of skin-microbiota system. This model was based on activation of Toll-Like Receptors in keratinocytes. TLR are membrane receptors which recognize conserved molecules from microbes and alert the immune system when activated. ArL was able to protect keratinocytes from TRL-induced IL-8 and hBD2 overproduction and thus to regulate inflammation in such conditions.

A disequilibrium in skin microbiota such as Propionibacterium acnes proliferation can also induce skin inflammation, on one hand by inducing lipid production by sebocytes, and on the other hand by producing lipase. ArL was able to reduce lipid droplet formation in a model of stimulated sebocytes and demonstrated an anti-lipase activity in tubo. These results corroborated the ability of ArL to modulate inflammation induced by microbiota imbalance. Finally, in a clinical study performed on human volunteers with sensitive skin submitted to an irritation stress, we could observe a soothing effect of ArL-containing formula in comparison with placebo, by reducing skin redness and stinging/burning sensations after 14 days of product application. In another clinical study, we could observe by corneometry a moisturizing effect of ArL-containing formula in comparison with placebo after 7 and 21 days of application. In conclusion, ArL can promote balance and comfort of reactive skins, likely by strengthening skin barrier and contributing to microbiota balance.

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