Gene Array Expression Profiling in Acne Lesions Reveals Marked Upregulation of Genes Involved in Inflammation and Matrix Remodeling

• Published in: Journal of investigative dermatology Vol. 126; no. 5; pp. 1071 - 1079
• Main Authors: Trivedi, Nishit R., Gilliland, Kathryn L., Zhao, Wei, Liu, Wenlei, Thiboutot, Diane M.
• Format: Journal Article
• Language: English
• Published: Danvers, MA Elsevier Inc 01-05-2006; Nature Publishing; Elsevier Limited
• Subjects: Acne Vulgaris - metabolism; Adolescent; Adult; beta-Defensins - genetics; Biological and medical sciences; Dermatology; Gene Expression Profiling; Gene Expression Regulation; Granzymes; Humans; Immunohistochemistry; Inflammation - metabolism; Inflammation Mediators - metabolism; Matrix Metalloproteinases - genetics; Medical sciences; Middle Aged; Multigene Family; Oligonucleotide Array Sequence Analysis; Polymerase Chain Reaction; Serine Endopeptidases - genetics; Signal Transduction; Skin involvement in other diseases. Miscellaneous. General aspects; Up-Regulation; Human; Skin disease; Gene; Dermatology; Acne; Genetics; Extracellular matrix; Inflammation; Remodeling; Gene expression profile
• ISSN: 0022-202X; 1523-1747
• DOI: 10.1038/sj.jid.5700213

The pathogenesis of acne has been linked to multiple factors such as increased sebum production, inflammation, follicular hyperkeratinization, and the action of Propionibacterium acnes within the follicle. In an attempt to understand the specific genes involved in inflammatory acne, we performed gene expression profiling in acne patients. Skin biopsies were obtained from an inflammatory papule and from normal skin in six patients with acne. Biopsies were also taken from normal skin of six subjects without acne. Gene array expression profiling was conducted using Affymetrix HG-U133A 2.0 arrays comparing lesional to nonlesional skin in acne patients and comparing nonlesional skin from acne patients to skin from normal subjects. Within the acne patients, 211 genes are upregulated in lesional skin compared to nonlesional skin. A significant proportion of these genes are involved in pathways that regulate inflammation and extracellular matrix remodeling, and they include matrix metalloproteinases 1 and 3, IL-8, human β-defensin 4, and granzyme B. These data indicate a prominent role of matrix metalloproteinases, inflammatory cytokines, and antimicrobial peptides in acne lesions. These studies are the first describing the comprehensive changes in gene expression in inflammatory acne lesions and are valuable in identifying potential therapeutic targets in inflammatory acne.