JEAN-MARIE BOTTO*, CHRISTELLE PLAZA, CELINE MEYRIGNAC, CHRISTOPHE CAPALLERE
*Corresponding author
Ashland, Global Skin Research Center, Sophia-Antipolis, France

Abstract

Acne vulgaris is the most common skin condition in developed countries, with a prevalence of 85% among adolescents and young adults. Acne is a complex multifactorial disease of the pilosebaceous follicle characterized by comedones, papules, pustules, and nodules that leave physical as well as psychological scars. The main pathogenic factors associated with acne development are follicular hyperkeratinization, increased sebum excretion and composition, Propionibacterium acnes colonization, and inflammation. In this study, we developed a model in silico describing the aspects of acne pathophysiology and testing models in vitro based on tissue engineering to explore isolated aspects of acne, such as the impact on pro-inflammatory cytokine release upon P. acnes application and its link with skin pigmentation. Other triggers related to extrinsic skin aging, e.g., particulate matter pollution, can induce inflammation in vitro, suggesting a possible role in modulating skin pigmentation.

INTRODUCTION

Skin aging is associated with phenotypic changes in cutaneous structures, and with various features such as impaired barrier function, localized hyperpigmentation (age spots), lower resistance to oxidative stress and DNA damage, decreased extracellular matrix protein synthesis, and the accumulation of senescent cells expressing markers of aging (senescence-associated beta-galactosidase, etc.). The accumulation of senescent cells with age is a hallmark of skin aging (1). Senescent cells develop a senescence-associated secretory phenotype (SASP) that impacts the surrounding environment and accelerates tissue aging by the release of pro-geronic factors (inflammatory cytokines, proteases…), contributing to low-level chronic inflammation of the tissue (inflammaging) (2). Besides the intrinsic aging program (chronological aging), external stimuli, such as exposure to sun light or environmental pollution, contribute to accelerate deleterious effects on skin tissue by enhancing oxidative stress, DNA damage, and inflammation (3), leading to accelerated skin aging and the appearance of localized hyperpigmentary lesions known as age-spots (solar lentigines) (4 ...