In vitro immunological and regenerative abilities of a dermocosmetic product: possible effects in atopic dermatitis

Author: Samara Eberlin

Published at: October 27, 2014

28th IFSCC Congress (International Federation of Societies of Cosmetic Chemists); Paris, October 27-28, 2014.
Polettini AJ, Eberlin S, Costa A, Pereira AFC, Dolis E, Torloni LBO.

Atopic dermatitis (AD) is a chronic inflammatory skin disease in which hereditary, environmental, and immunological factors play a major role. Characterized by xerosis, eczematous lesions, and pruritus, AD changes between two phases: an acute Th2 predominant state with its cytokine pattern up-regulating IgE, and a chronic AD phase with Th1 cytokines, predominantly interferon-γ (IFN-γ) and interleukin-12 (IL-12), that down-regulate IgE. It is important to note that pruritus usually leads to an "itch-scratch" cycle that may compromise the epidermal barrier, dermis architecture, and function, resulting in transepidermal water loss and defective wound healing. The wound signature of AD is the proliferation of progenitor cells leading to epidermal hyperplasia, and tissue remodeling resulting in the development of spongiosis. In this study, we evaluated the anti-inflammatory and regenerative properties of a cosmetic product through quantification of IFN-γ, interleukin-12, and TGF-β using an ex vivo model of human skin. We also assessed wound healing ability by measurement of transforming growth factor beta (TGF-β) and cell migration using an in vitro model of human fibroblast culture. The synthesis of IL-12, IFN-γ, and TGF-β were measured using human skin explants obtained from plastic surgery. This study was carried out with the approval of the Ethics Committee. Incubation of skin explants with IL-1β promoted increases of 42.2% in the production of IFN-γ. Concurrent treatment of skin explants with the test product prevented the increase of inflammatory cytokines, reaching up to a 48.5% reduction compared to the IL-1β-stressed group. IL-1β stimulation did not produce increases in the amount of IL-12; however, the test product reduced the synthesis of this cytokine to undetectable levels compared to the basal control group. The synthesis of TGF-β was significantly decreased by the addition of IL-1β in cultured skin ex vivo. Conversely, the test product was able to promote a 1.9-fold increase in the synthesis of TGF-β when compared to the IL-1β-stressed group. The increase in the production of this growth factor corroborates the results obtained in the cell migration assay, where the test product was able to increase cell migration compared to the control group. After 48 hours, the scratch was completely filled, similarly to the group stimulated with TGF-β. AD is associated with hyperresponsiveness of lymphocytes to allergens. In acute AD, only Th2-type lymphocytes are activated, whereas in more chronic forms of AD, the activity of both Th1- and Th2-type lymphocytes increases. Th1 cytokines IL-12 and IFN-γ are present in the chronic phase of AD and are responsible for the perpetuation of the inflammatory state, culminating in connective tissue damage. A third group of cytokines, which includes TGF-β1 and IL-10, have general immunosuppressive activity, blocking both Th1- and Th2-type cytokine activity. In this work, it was demonstrated that the test product exerts a protective effect against inflammatory and immunological imbalance induced by IL-1β in human skin explants. The results also showed the ability of the test product to stimulate TGF-β1 and fibroblast migration, both involved in the wound healing process. Taken together, these data suggest that the test product might be considered an effective skin care formulation for atopic skin.