BackgroundAcne vulgaris has been linked to the Western diet. Hyperglycemic diet increases insulin and insulin-like growth factor (IGF)-1. Deeper insights into IGF-1-mediated signal pathway are critical importance to understand the impact of Western diet.ObjectiveWe investigated the effect of IGF-1 on the expression of inflammatory biomarkers and sebum production in cultured sebocytes.MethodsPolymerase chain reaction and enzyme-linked immunosorbent assay were performed to measure changes in the expression of inflammatory biomarkers including interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor (TNF)-α, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), IGF1R, IGFBP2, sterol response element-binding protein (SREBP), and phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha (PI3KCA) after the treatment of cultured sebocytes with 10−7 M or 10−5 M IGF-1. Sebum production was evaluated after the treatment of cultured sebocytes with 10−7 M or 10−5 M IGF-1 using lipid analysis.ResultsThe expression levels of IL-1β, IL-6, IL-8, and TNF-α in cultured sebocytes after treatment with 10−7 M or 10−5 M IGF-1 were increased. Increased gene expression levels of NF-κB in cultured sebocytes were also shown after 10−7 M or 10−5 M IGF-1 treatments. Gene expression of these inflammatory biomarkers was decreased after 10−7 M or 10−5 M IGF-1 treatment in the presence of 100 nM NF-κB inhibitor. Treatment with 10−7 M or 10−5 M IGF-1 increased the gene expression levels of IGF1R, IGFBP2, SREBP and PI3KCA in cultured sebocytes. Sebum production from cultured sebocytes treated with 10−7 M or 10−5 M IGF-1 was also increased.ConclusionIt is suggestive that IGF-1 might be involved in the pathogenesis of acne by increasing both expression of inflammatory biomarkers and also sebum production in sebocytes.

Background:Inflammatory cytokines are the key factor in the pathophysiology of acne. It is well known that keratinocytes synthesize many kinds of inflammatory cytokines. In addition, it is reported that inflammatory cytokines are also expressed from sebocytes, which originate from the same stem cells with keratinocytes.Aim:To clarify changes in the expression of inflammatory biomarkers from cultured sebocytes after treatment with vitamin D.Materials and Methods:Reverse transcription-polymerase chain reaction (RT-PCR) was done to measure changes in the expression of inflammatory biomarkers, including interleukin-1β (IL-1β), IL-6, IL-8, and tumor necrosis factor-α (TNF-α), and several subtypes of matrix metalloproteinases (MMPs) after treatment of a group of cultured sebocytes with vitamin D. Vitamin D receptor (VDR) small interfering RNA (siRNA) was added in the other group of cultured sebocytes to assure the role of vitamin D on the expression of inflammatory biomarkers. Enzyme-linked immunosorbent assay (ELISA) was also performed in the vitamin D-treated sebocytes.Results:Cultured sebocytes showed non-significant changes in the gene expression of inflammatory biomarkers after treatment with vitamin D. In cultured sebocytes treated with a VDR siRNA, the expression of inflammatory biomarkers was not blocked after treatment with vitamin D. ELISA showed a significant decrease in the expression of IL-6, IL-8, and MMP-9, but a significant increase in the expression of MMP-1 and MMP-3, after treatment with vitamin D (10-6 M).Conclusion:Expression of inflammatory biomarkers is influenced by treatment with vitamin D in cultured sebocytes, but not through VDR.

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Sebaceous gland hyperplasia and increased sebum secretion after irradiation of ultraviolet (UV)-B has been widely accepted. This study was performed to clarify expression of inflammatory cytokines after irradiating UV-B in cultured sebocytes. Reverse transcription polymerase chain reaction was performed to measure gene expression of inflammatory cytokines, including interleukin (IL)-1β, IL-6, IL-8 and tumor necrosis factor-α, in cultured sebocytes after exposure to 40 and 70 mJ/cm(2) UV-B. Protein expression of inflammatory cytokines and lipid production in cultured sebocytes after exposure to UV-B were measured using enzyme-linked immunoassay and lipid analysis kit. The expression of inflammatory cytokines, especially IL-1β and IL-8, was significantly increased in cultured sebocytes after treatment with UV-B. Many more studies on the effect of UV-B on sebaceous glands should be performed to reveal the pathogenic mechanism of acne.

Background: Although photodynamic therapy (PDT) is widely performed for acne, little is known about its exact therapeutic mechanism. Objective: We aimed to estimate the efficacy and safety of PDT on acne and to discover its mode of action. Methods: We performed PDT on 12 patients with mild to moderate acne. The clinical efficacy was assessed by counting the acne lesions and measuring the sebum secretion before and after PDT. In addition, we took biopsy samples from the peri-lesional areas before and after 3-session of PDT. To examine the degree of apoptosis of the sebaceous follicles, TUNEL assay was performed. To investigate the changes of toll-like receptor (TLR)-2 and TLR-4 expression after PDT, immunohistochemical stainings were also carried out. Finally, we performed TUNEL assay using the cultured sebocytes to confirm the apoptosis of sebocytes in vitro after PDT. Results: There was a significant reduction in the number of inflammatory acne lesions after PDT, compared to baseline (p＜0.05). Sebum excretion significantly decreased 2 weeks after the first PDT session except for one patient (p＜0.05). The TUNEL positive cells in the peri-lesional sebaceous glands after PDT markedly increased, compared with those of before PDT. A decrease in TLR-2 and TLR-4 expression by sebaceous glands and epidermis after PDT was 50% and 30%, respectively. Conclusion:Our results demonstrate that apoptosis of the sebaceous glands is associated with improvement of acne by PDT. PDT has shown to down-regulate TLR-2 and TLR-4 expression in the sebaceous glands and epidermis of acne patients. (Ann Dermatol 23(1) 23∼32, 2011)