کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5649785 | 1407131 | 2017 | 31 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Allergy-Inducing Chromium Compounds Trigger Potent Innate Immune Stimulation Via ROS-Dependent Inflammasome Activation
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کلمات کلیدی
DAMPNHEKMrOSBMDCTLR12-O-tetradecanoylphorbol-13-acetatetPALPSCr3+ - Cr3 +Adenosine Triphosphate - آدنوزین تری فسفاتATP - آدنوزین تری فسفات یا ATPdamage-associated molecular pattern - الگوی مولکولی مرتبط با آسیبToll-like receptor - تیالآرPotassium dichromate - دی کرومات پتاسیمbone marrow-derived dendritic cell - سلول های دندانیایی حاصل از استخوان مغز استخوانlactate dehydrogenase - لاکتات دهیدروژناز LDH - لاکتات دهیدروژناز به صورت مختصر شده LDH lipopolysaccharide - لیپوپلی ساکاریدNormal human epidermal keratinocyte - کراتینوسیت اپیدرمی طبیعی انسانChromium (III) - کروم (III)Chromium (VI) - کروم (VI)trivalent chromium - کروم سه گانهHexavalent chromium - کروم شش ظرفیتیPotassium chromate - کرومات پتاسیمChromium chloride - کلرید کرومmitochondrial reactive oxygen species - گونه های اکسیژن واکنش پذیر میتوکندری
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
امراض پوستی
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![عکس صفحه اول مقاله: Allergy-Inducing Chromium Compounds Trigger Potent Innate Immune Stimulation Via ROS-Dependent Inflammasome Activation Allergy-Inducing Chromium Compounds Trigger Potent Innate Immune Stimulation Via ROS-Dependent Inflammasome Activation](/preview/png/5649785.png)
چکیده انگلیسی
Chromium allergy is a common occupational skin disease mediated by chromium (VI)-specific T cells that induce delayed-type hypersensitivity in sensitized individuals. Additionally, chromium (VI) can act as an irritant. Both responses critically require innate immune activation, but if and how chromium (VI) elicits this signal is currently unclear. Using human monocytes, primary human keratinocytes, and murine dendritic cells we show that chromium (VI) compounds fail to trigger direct proinflammatory activation but potently induce processing and secretion of IL-1β. IL-1β release required priming by phorbol-ester or toll-like receptor stimulation and was prevented by inhibition of K+ efflux, NLRP3 depletion or caspase-1 inhibition, identifying chromium (VI) as a hapten activator of the NLRP3 inflammasome. Inflammasome activation was initiated by mitochondrial reactive oxygen species production triggered by chromium (VI), as indicated by sensitivity to treatment with the ROS scavenger N-acetyl cysteine and a coinciding failure of K+ efflux, caspase-1, or NLRP3 inhibition to prevent mitochondrial reactive oxygen species accumulation. IL-1β release further correlated with cytotoxicity that was secondary to reactive oxygen species, K+ efflux, and NLRP3 activation. Trivalent chromium was unable to induce mitochondrial reactive oxygen species production, inflammasome activation, and cytotoxicity, suggesting that oxidation state-specific differences in mitochondrial reactivity may determine inflammasome activation and allergic/irritant capacity of different chromium compounds.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Investigative Dermatology - Volume 137, Issue 2, February 2017, Pages 367-376
Journal: Journal of Investigative Dermatology - Volume 137, Issue 2, February 2017, Pages 367-376
نویسندگان
Christian Adam, Jonas Wohlfarth, Maike HauÃmann, Helga Sennefelder, Annette Rodin, Mareike Maler, Stefan F. Martin, Matthias Goebeler, Marc Schmidt,