1228 Actinic lentigines from European and Japanese volunteers are characterized by a molecular and cellular inflammatory micro-environment

Abstract

Actinic lentigines (AL), also called age spots, are benign skin hyperpigmented lesions associated with age and chronic sun exposure. Despite their high prevalence in elderly people, the biological events underlying the development of these lesions remain unclear. In order to better understand the pathophysiological characteristics of AL, we characterized the inflammation response in AL from European and Japanese volunteers, by analyzing the gene expression profile associated with inflammation and by immunostaining of inflammatory/immune cells in skin sections. Results showed that a large number of genes associated with inflammation/immune response were altered in AL versus adjacent non lesional skin (NL) representing ∼10% of total modulated genes. These genes were modulated in the same way in the two populations and indicate a proinflammatory process as attested by the activation of arachidonic acid pathway including PTGS2 (COX2). Furthermore, the overexpression of chemokines genes suggests that chemoattraction of inflammatory cells could take place in AL. To verify this, immunostaining of several cellular subsets was performed and revealed the increase of antigen-presenting cells (HLA-DR +), macrophages (CD68+) and CD4+ T-cells in the dermis of AL vs NL, which strengthens a chemoattraction role in the physiopathology of AL. Consequently, prostaglandins and chemokines release associated with the infiltration of inflammatory cells could contribute to the self-maintenance of an inflammatory microenvironment in AL which may alter skin homeostasis and pigmentation. Normalizing skin by targeting this inflammatory loop could help for efficient and long-term treatment of age spots.