کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3213977 1203262 2009 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Nicotinamide inhibits Propionibacterium acnes-induced IL-8 production in keratinocytes through the NF-κB and MAPK pathways
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی امراض پوستی
پیش نمایش صفحه اول مقاله
Nicotinamide inhibits Propionibacterium acnes-induced IL-8 production in keratinocytes through the NF-κB and MAPK pathways
چکیده انگلیسی

BackgroundPropionibacterium acnes (P. acnes) has been implicated in the inflammatory phase of acne vulgaris. It has been shown to activate interleukin-8 (IL-8) secretion by interacting with Toll-like receptor 2 (TLR-2) on the surface of keratinocytes. Nicotinamide has been shown to be an effective treatment for skin inflammation in various conditions, including acne vulgaris.ObjectiveTo investigate the molecular mechanisms underlying the anti-inflammatory properties of nicotinamide in keratinocytes stimulated by P. acnes.MethodsHaCaT cells and primary keratinocyte cell lines were stimulated by P. acnes in the presence of nicotinamide. IL-8 production was monitored by ELISA on the cell culture supernatant and by qRT-PCR on total RNA extract. A luciferase reporter system assay was used to assess nicotinamide activity with the IL-8 promoter in transfected keratinocytes. We used western blotting to analyze the effect of nicotinamide on activation of the NF-κB and MAPK pathways.ResultsNicotinamide significantly decreased IL-8 production in a dose-dependent manner, decreasing both mRNA and protein levels for this chemokine in immortalized HaCaT cells and primary keratinocytes. P. acnes-induced IL-8 promoter activation seemed to be downregulated by nicotinamide, which inhibited IκB degradation and the phosphorylation of ERK and JNK MAP kinases.ConclusionOur results indicate that nicotinamide inhibits IL-8 production through the NF-κB and MAPK pathways in an in vitro keratinocytes/P. acnes model of inflammation. Keratinocytes involved in the innate immune response may be a suitable target for treatment during the early phase of inflammation.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Dermatological Science - Volume 56, Issue 2, November 2009, Pages 106–112
نویسندگان
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