LB1556 miR-10a modulates keratinocyte responses in atopic dermatitis

Abstract

Atmospheric factors such as air pollution have been implicated in premature skin aging and also being associated with several skin pathologies. Among the pollutants to which cutaneous tissues is daily exposed, ozone has been shown to be one of the most noxious. The skin damage caused by ozone exposure is largely related to its ability to generate a complex cascade of oxidative stress related reactions. Indeed ozone is not able to penetrate the skin and although it is not a radical per se it is able to react with the stratum corneum fatty acids and generate oxidized lipids that can act as second messengers. This cascade of effects is able to initiate a pro-inflammatory skin response that, with the altered redox homeostasis, leads to a vicious cycle where inflammation and ROS aliment each other. In this contest the fine regulated balance between NFkB and Nrf2 activation is also compromise and the defensive ability of cutaneous cells is corrupted. In addition, the insufficient activation of NRF2 lead to the arousal of the inflammasome pathway that can eventually lead to cells damage and death. The action by which ozone affect skin has been evidenced in several cutaneous model (2D, 3D, biopsies) and also in human subjects. Therefore, knowing the exact mechanism by which ozone is able to affect skin can bring new insights on possible therapeutic and preventive interventions.