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Accession IconGSE108110

Long-acting immune responses including plasma cells and alteration of sebaceous glands cause atrophic scar formation in acne patients

Organism Icon Homo sapiens
Sample Icon 53 Downloadable Samples
Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

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Background: Possible outcomes of acne lesions are atrophic scars which may cause serious physical and psychological distress. Current treatments of post-acne scarring remain difficult and often require invasive procedures. Pathophysiological studies on acne scaring investigated only the first week of papule life. Objectives: Study the pathophysiology of atrophic acne scar formation to identify molecular and cellular pathways that can lead to new therapies for the prevention of acne scarring. Methods: Large-scale gene expression profiling of uninvolved acne skin and acne papules of 48 hours and 3 weeks of age, respectively, of both, scar-prone (SP) and non-scar-prone (NSP) patients was performed. Immunohistochemistry techniques were applied to confirm transcriptomics results on the protein and cellular level. Results: Gene expression and immunohistochemistry analyses showed a very similar immune response in 48 hours-old papules in 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 genes related to lipid metabolism was observed in 48 hours-old papules in NSP patients, followed by normalization of gene expression levels after 3 weeks. In contrast, in SP patients a drastic reduction of lipid metabolizing enzymes was observed in 3 week-old papules, suggesting irreversible modifications. The affected lipid metabolism genes were found preferentially expressed in human sebaceous glands, pointing to a destruction of sebaceous gland structures after 3 weeks of inflammatory remodelling in SP acne patients.
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