Excessive sebum production secondary to sebaceous gland hyperplasia is the first abnormality to occur in IAV [13]. Subsequent hyperkeratinization of the hair follicle prevents normal shedding of the follicular keratinocytes, obstructing the follicle forming an inapparent microcomedo. Lipids and cellular debris accumulate within the blocked follicle [14]. This microenvironment encourages colonization of P. acne, which provokes an immune response through the production of numerous inflammatory mediators. Inflammation is further enhanced by follicular rupture and subsequent leakage of lipids, bacteria and fatty acids into the dermis.
Data from this study points out to altered immunoreactivity of IL-8 in the lesional skin of acne patients. This was highlighted by the increased expression in IAV skin biopsies compared to normal ones. Increased immunoreactivity was significantly associated with epidermal hyperplasia, follicular hyperkeratosis. In addition, the more pronounced IL-8 expression of the endothelial cells and neutrophilic infiltrate correlated with the extent of dermal inflammatory response and dermal angiogenesis. This expression is concordant with previous studies showing that IL-8 is released by a variety of cell types including monocytes, macrophages, T lymphocytes, fibroblasts, endothelial cells and keratinocytes in response to inflammatory stimulus [4,15,16]. Epidermal hyperplasia and follicular hyperkeratosis secondary to IL-8 production have been noted in psoriatic skin [17]. Early studies on IL-8 point out to its inflammatory nature as a chemokine that attracts and degranulates neutrophils [18,19]. This degranulation release potential key regulators of cell signalling during inflammation such as serine proteases, cathepsin G, leucocyte elastase and proteinase at sites of inflammation, triggering IL-8 and subsequently activate different IL-8 receptors [20].
Contrary to other studies [14,21], IL-8 was mildly expressed in normal keratinocytes in non lesional biopsies in two cases while it was absent in the rest. This may be related to the antibody clone used in the present study. In fact, the pattern of staining was different depending on the clone used in the study of Sticherling et al [15], where suprabasal keratinocytes were staining with 52E8 and all keratinocytes were reactive with 46E5. However, the mild or lack of expression of IL-8 in normal keratinocytes in the present work points to its role in mediating and participating to the inflammatory response in IAV cases.
It has been suggested that local changes in the peripheral blood vessels at the dermal papilla or in the interfollicular region may play a role in evolution of IAV because blood vessels can deliver proinflammatory cytokines that modulated a range of inflammatory and proliferative processes [16]. IL-8 may be a potential endothelial cell growth and survival factor, interacting through its receptors expressed by endothelial cells. The mechanism of IL-8 regulation of angiogenesis may be in part due to enhanced proliferation and survival of endothelial cells by differential expression of antiapoptosis genes and in part by activation of matrix metalloproteinases 2 and 9 [16]. This point is supported in the present study by an increase in endothelial cells IHC expression of IL-8 and increased dermal blood vessels in the skin biopsies of IAV patients.
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