Atrophic scar formation in acne patients involves long-acting immune responses with plasma cells and alteration of sebaceous glands

BACKGROUND: Possible outcomes of acne lesions are atrophic scarswhich may cause serious psychological distress. Current treatments of post-acne scarringoften require invasive procedures. Pathophysiological studies on acne scarringinvestigated only the first week of papulelife. OBJECTIVES: Study the pathophysiology of atrophic scarformation to identify molecular and cellular pathways that can lead to new therapies for the prevention of acne scarring. METHODS: Large-scale gene expression profiling and immunohistochemistry analysis were performed on uninvolved skin and papulesin both, scar-prone (SP) and non- scar-prone (NSP) acne patients, at different time points. RESULTS: Gene expression and immunohistochemistry analyses showed a very similar immune response in 48 hours-old papulesin SP and NSP populations, characterized by elevated numbers of T cells, neutrophils and macrophages. However, only in SP patients the immune response persisted in 3 week-old papules, and was characterized by an important infiltrate of B cells. Transient down-modulation of sebaceous glandmarkers related to lipid metabolism was observed in 48 hours-old papulesin NSP patients, followed by normalization after 3 weeks. In contrast, in SP patients a drastic reduction of these markers persisted in 3 week-old papules, suggesting an irreversible destruction of sebaceous glandstructures after inflammatory remodelling in SP acne patients. CONCLUSIONS: Long lived acne papulesare characterized by a B cell infiltrate. A relationship exists between the duration and severity of inflammation and the alteration of sebaceous glandstructures, leading to atrophic scarformation in acne. This article is protected by copyright. All rights reserved.