Investigating the interplay of the immune system, skin barrier, and microbiome following dermal exposure to triclosan

Triclosan is an antimicrobial chemical used in healthcare products that are applied to the skin. However, exposure to triclosan has been positively associated with food allergy, aeroallergy, and asthma severity in humans. In mice, dermal triclosan exposure, although not directly sensitizing, has been shown to augment the allergic response in a model of asthma. Furthermore, exposure to triclosan on mouse skin has been demonstrated to be immunomodulatory through the activity of thymic stromal lymphopoietin and S100 calcium-binding protein A8. The skin barrier and microbiome are known to interact with the immune system and disruptions in barrier integrity and the microbiome are associated with allergic diseases. However, the impact of dermal triclosan exposure on the skin integrity, skin microbiome, and its interplay with the immune system has not been evaluated. In these studies, dermal exposure to triclosan was evaluated using a mouse model and a model of reconstructed human epidermis. In mice, repeated (7-day) dermal exposure to 2% triclosan increased transepidermal water loss, altered the expression patterns of skin barrier genes, and changed the composition of the skin and gut microbiome. In a model of reconstructed human epidermis, exposure to 0.2% triclosan increased skin permeability, altered the expression of skin barrier genes, and increased the production of proinflammatory cytokines. Taken together, these results suggest that exposure to triclosan disrupts the skin barrier integrity and microbiome and that these alterations may influence immune responses. A better understanding of immunomodulation and its contribution to the development of allergic disease is needed to aid in the prevention and treatment of disease.