Inflammatory Events Are Involved in Acne Lesion Initiation

University of Leeds, and Leeds General Infirmary, Leeds, UK.
Journal of Investigative Dermatology (Impact Factor: 7.22). 08/2003; 121(1):20-7. DOI: 10.1046/j.1523-1747.2003.12321.x
Source: PubMed


The earliest subclinical acne "lesion" is a microcomedone, of which hyperproliferation of the follicular epithelium is a characteristic feature. Inflammatory cells have been observed at the periphery of these "lesions". This study investigated whether inflammatory events occur pre or post hyperproliferative changes. Cellular, vascular, and proliferative markers were examined by immunohistochemical techniques on biopsies of clinically normal follicles from uninvolved skin and early inflamed lesions from acne patients. Control follicles were obtained from non-acne subjects. Follicles from uninvolved skin exhibited no microcomedonal features. Proliferation in the epithelium was comparable to controls and was significantly lower than in inflamed lesions. Numbers of CD3+, CD4+ T cells were elevated in the perifollicular and papillary dermis although levels were not equivalent to those in papules. The number of macrophages was also greatly increased and similar to those in papules. There were no changes in blood vessel numbers or vascular intercellular adhesion molecule 1 expression but E-selectin expression was increased to levels found in papules and vascular adhesion molecule 1 levels were upregulated. Levels of the pro-inflammatory cytokine interleukin-1 were also upregulated perifollicularly. Moreover, aberrant integrin expression was demonstrated in the epidermis around these uninvolved follicles and inflamed lesions whereas the basement membrane was still intact. These results provide novel evidence for vascular endothelial cell activation and involvement of inflammatory responses in the very earliest stages of acne lesion development.

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Available from: Kathryn Thomson, Feb 10, 2015
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    • "acnes) within the follicle, and inflammation. The earliest change in the pilosebaceous unit was initially thought to be follicular hyperkeratinization, which is associated with both increased proliferation and decreased desquamation of keratinocytes lining the follicular orifice [8]. Initiating factors for this inflammatory process are unknown. "
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    ABSTRACT: Acne vulgaris is the most common cutaneous disorder affecting adolescents and young adults. Some studies have reported an association between serum zinc levels and acne vulgaris. We aimed to evaluate the serum zinc level in patients with acne vulgaris and compare it with healthy controls. One hundred patients with acne vulgaris and 100 healthy controls were referred to our clinic. Acne severity was classified according to Global Acne Grading System (GAGS). Atomic absorption spectrophotometry was used to measure serum zinc levels. Mean serum level of zinc in acne patients and controls was 81.31 ± 17.63 μg/dl and 82.63 ± 17.49 μg/dl, respectively. Although the mean serum zinc level was lower in acne group, it was not statistically significant ( P = 0.598 ). There was a correlation between serum zinc levels with severity and type of acne lesions. The results of our study suggest that zinc levels may be related to the severity and type of acne lesions in patients with acne vulgaris. Relative decrease of serum zinc level in acne patients suggests a role for zinc in the pathogenesis of acne vulgaris.
    Full-text · Article · Jul 2014 · BioMed Research International
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    • "Surprisingly, in early acne lesions, infiltrating cells consist mainly of CD4 þ T cells (Norris and Cunliffe, 1988; Layton et al., 1998). These memory/effector CD4 þ T cells are detected in close proximity to macrophages and are also present in uninvolved follicles from acne patients but not in non-acne controls (Jeremy et al., 2003). In addition, P. acnes has been shown to induce T-cell proliferation (Jappe et al., 2002), and reactive P. acnes-specific CD4 þ T cells have been isolated from early inflamed acne lesions (Mouser et al., 2003). "
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    ABSTRACT: Propionibacterium acnes is a Gram-positive commensal bacterium thought to be involved in the pathogenesis of acne vulgaris. While the ability of P. acnes in the initiation of pro-inflammatory responses is well documented, little is known about adaptive immune responses to this bacterium. The observation that infiltrating immune cells consist mainly of CD4(+) T cells in the perifollicular space of early acne lesions suggests that helper T cells may be involved in immune responses caused by the intra-follicular colonization of P. acnes. A recent report showing that P. acnes can induce IL-17 production by T cells suggests that acne might be a Th17-mediated disease. In line with this, we show in this work that, in addition to IL-17 A both Th1 and Th17 effector cytokines, transcription factors and chemokine receptors are strongly upregulated in acne lesions. Furthermore, we found that, in addition to Th17, P. acnes can promote mixed Th17/Th1 responses by inducing the concomitant secretion of IL-17 A and IFNγ from specific CD4(+) T cells in vitro. Finally, we show that both P. acnes-specific Th17 and Th17/Th1 cells can be found in the peripheral blood of patients suffering from acne and, at lower frequencies, in healthy individuals. We therefore identified P. acnes-responding Th17/Th1 cells as previously unreported CD4(+) sub-population involved in inflammatory acne.Journal of Investigative Dermatology accepted article preview online, 10 July 2014; doi:10.1038/jid.2014.290.
    Full-text · Article · Jul 2014 · Journal of Investigative Dermatology
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    • "follicular hyperkeratosis [7] [8] [9], SB hyperproduction [3] [10] [11], and periglandular dermal inflammation [12]. LA is present in acyl-glycosyl ceramides; hence, it participates in the maintenance of the skin barrier [13]. "
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