Acne vulgaris is a chronic inflammatory disease of the pilosebaceous units characterized by the formation of comedones, erythrematous papules and pustules, less frequently by nodules or pseudocyts [1]. It is a pleomorphic disorder with multifactorial pathogenesis [2]. Acne has a significant economic and social impact as well as a negative effect on self-image and outlook, especially during the emotionally critical period of adolescence [3]. Propionibacterium acnes (P. acnes), an anaerobic pathogen plays an important role in the pathogenesis by triggering the proinflammatory mediators [4,5] through activation of Toll-like receptors 2 (TLR2) [6-8]. Among these mediators, IL-8 originally identified as neutrophil-activating peptide-1 [9], along with P. acnes induce chemotactic factors that play a role in attracting neutrophils to the pilosebaceous unit (6, 7, 8). The production of IL-8 by P. acnes is through activation of the NF-kappa B [10]. Gene array expression profiling in acne lesions reveals marked upregulation of genes, including IL-8, involved in inflammation and matrix remodelling [11].
To our knowledge, no reports evaluated the IL-8 IHC expression in skin biopsies of inflammatory acne. Therefore, this study was conducted to assess this expression and to correlate it with disease severity and histological changes in an attempt to understand the disease pathogenesis. The elucidation of this role may highlight the potential role of IL-8 in therapeutic targets in inflammatory acne.
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