Original Article

Subject Categories: Immunology/Infection

Journal of Investigative Dermatology (2006) 126, 1071–1079. doi:10.1038/sj.jid.5700213; published online 9 March 2006

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

Nishit R Trivedi1,4, Kathryn L Gilliland1,4, Wei Zhao2, Wenlei Liu2 and Diane M Thiboutot1,3

  1. 1The Jake Gittlen Cancer Research Foundation, The Pennsylvania State University College of Medicine, Hershey, Pennsylvania, USA
  2. 2Department of Health Evaluation Sciences, The Pennsylvania State University College of Medicine, Hershey, Pennsylvania, USA
  3. 3Department of Dermatology, The Pennsylvania State University College of Medicine, Hershey, Pennsylvania, USA

Correspondence: Dr Diane M. Thiboutot, Department of Dermatology, UPC-2 Rm 4300, The Pennsylvania State University College of Medicine, 500 University Drive, Hershey, Pennsylvania 17033, USA. E-mail: dthiboutot@psu.edu

4These authors contributed equally to this work

Received 9 October 2005; Revised 10 December 2005; Accepted 3 January 2006; Published online 9 March 2006.

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Abstract

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 beta-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.

Abbreviations:

DEFB1, DEFB2, DEFB3, DEFB4, human beta-defensin 1, 2, 3, 4; MMP-1, MMP-3, matrix metalloproteinase 1, 3

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