Findings from large epidemiologic studies indicate that there is a link between smoking and extrinsic skin ageing. We previously reported that matrix metalloproteinases (MMPs) mediate connective tissue damage in skin exposed to tobacco smoke extracts. Tobacco smoke contains more than 3800 constituents, including numerous water-insoluble polycyclic aromatic hydrocarbons (PAHs) that trigger aryl hydrocarbon receptor (AhR) signalling pathways. To analyse the molecular mechanisms involved in tobacco smoke-induced skin ageing, we exposed primary human fibroblasts and keratinocytes to tobacco smoke extracts. Hexane- and water-soluble tobacco smoke extracts significantly induced MMP-1 mRNA in both human cultured fibroblasts and keratinocytes in a dose-dependent manner. To clarify the involvement of the AhR pathway, we used a stable AhR-knockdown HaCaT cell line. AhR knockdown abolished the increased transcription of the AhR-dependent genes CYP1A1/CYP1B1 and MMP-1 induced by either of the tobacco smoke extracts. Furthermore, the tobacco smoke extracts induced 7-ethoxyresorufin-O-deethylase activity, which was almost completely abolished by AhR knockdown. Likewise, treating fibroblasts with AhR pathway inhibitors, that is, the flavonoids 3-methoxy-4-nitroflavone and α-naphthoflavone, blocked the expression of CYP1B1 and MMP-1. These findings suggest that the tobacco smoke extracts induce MMP-1 expression in human fibroblasts and keratinocytes via activation of the AhR pathway. Thus, the AhR pathway may be pathogenetically involved in extrinsic skin ageing.

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based on the known additive or synergistic activity of AMP (23), it is likely that lactoferrin works together with the other AMP at the skin surface to provide an immune defense. Supporting InformationAdditional Supporting Information may be found in the online version of this article: Data S1. Functional classification of sweat proteins. Table S1. Proteome list from sweat by LC-MS ⁄ MS. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. Tobacco smoke is related to Th17 generation with clinical implications for psoriasis patientsKan Torii, Chiyo Saito, Takuya Furuhashi, Akiko Nishioka, Yoichi Shintani, Kana Kawashima, Hiroshi Kato and Akimichi Morita Department of Geriatric and Environmental Dermatology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan Correspondence: Kan Torii, Department of Geriatric and Environmental Dermatology, Nagoya City University Graduate School of Medical Sciences, 1-Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan, Tel.: +81-52-853-8261, Fax: +81-52-852-5449, e-mail: kan042033@live.jp Abstract: Environmental factors contribute to the increased prevalence of autoimmune diseases via T helper type-17 cell (Th17) activation. Tobacco smoking increases the risk of psoriasis, but the mechanisms are not clear. We evaluated the percentage of circulating Th17 among CD3 + cells in peripheral blood mononuclear cells (PBMC) obtained from 27 healthy volunteers (2.58 ± 0.80%), 33 smoker (3.55 ± 1.33%) and 21 non-smoker (3.10 ± 1.14%) patients with psoriasis to elucidate the relation between smoking and psoriasis. More smokers (19 ⁄ 33) than non-smokers (6 ⁄ 21) had high Th17 levels (Th17 ⁄ CD3 > 3.38%, mean + 1 SD of healthy volunteers). Tobacco smoke extract (TSE, 7 ll ⁄ ml) induced Th17 generation from central memory T cells in vitro. TSE increased interleukin 17 and 22 expression. These findings demonstrate the relation between tobacco smoke and IL-17 and IL-22, which exacerbate psoriasis.

This study investigated phototherapy-induced changes in certain adipokine levels in patients with psoriasis. Patients with psoriasis (n=36) were recruited and body mass index (BMI) and disease severity (Psoriasis Area and Severity Index) were recorded. Serum resistin and leptin levels before and after bath-psoralen and ultraviolet (UV) A or narrow-band UVB therapy were examined by enzyme-linked immunosorbent assay. Serum leptin levels correlated positively with BMI. Phototherapy induced no remarkable change in the leptin levels, but significantly decreased serum resistin levels from 9.02±8.83 to 4.86±3.30ng/ml. Serum resistin levels might be involved in insulin resistance and inflammation, and correlate with disease severity in patients with psoriasis. The reduction in serum resistin induced by phototherapy might be related to the clinical efficacy of this treatment for psoriasis.

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