Comprehensive analysis of phenotypes and transcriptome characteristics reveal important contribution of chronic stress and inflammation in the pathogenesis of acne.

Acne vulgaris is a common chronic inflammatory skin disorder with a multifactorial pathogenesis involving genetic predisposition, hormonal regulation, microbial factors, and the cutaneous immune microenvironment. In recent years, psychosocial influences and their association with acne onset and progression have drawn increasing attention. Chronic stress may disturb immune homeostasis via neuroendocrine regulatory pathways and thereby contribute to acne pathophysiology. However, the molecular mechanisms by which chronic stress modulates acne development and exacerbation remain unclear. In the present study, we established a chronic stress-induced murine model of acne to characterize stress-related behavioral alterations, skin histopathological changes, serum corticosterone levels, and inflammatory mediators profiles in both serum and skin tissue. We further performed transcriptomic profiling to identify differentially expressed genes and to elucidate candidate regulatory pathways and molecular targets. Our findings indicate that chronic stress indeed contributes to the pathological progression of acne. However, stress hormones do not appear to directly drive inflammatory worsening. Instead, transcriptomic analysis indicated that chronic stress may play an important role in complex neuroendocrine-metabolic-immune interactions involved in acne exacerbation. These preliminary results provide experimental evidence exploring the role of chronic stress in acne pathogenesis and suggest potential targets for acne prevention and treatment.