کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8337874 | 1540970 | 2018 | 19 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Vitamin D effects on monocytes' CCL-2, IL6 and CD14 transcription in Addison's disease and HLA susceptibility
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کلمات کلیدی
CYP27B1CCL-2GRERXRVDRERetinoid X receptorCD14IL6VDR1,25(OH)2D3 - 1،25 (OH) 2D325(OH)D3 - 25 (OH) D325-hydroxyvitamin D3 - 25 هیدروکسی ویتامین D3HLA - آنتیژن گلبول سفید انسانیAddison’s disease - بیماری آدیسونDendritic cell - سلول دندریتیکvitamin D response element - عنصر پاسخ ویتامین D استGlucocorticoid response element - عنصر پاسخ گلوکوکورتیکوئیدVitamin D - ویتامین دیhealthy controls - کنترل های سالمGlucocorticoids - گلوکوکورتیکوئیدهاVitamin D receptor - گیرنده ویتامین D
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Vitamin D effects on monocytes' CCL-2, IL6 and CD14 transcription in Addison's disease and HLA susceptibility Vitamin D effects on monocytes' CCL-2, IL6 and CD14 transcription in Addison's disease and HLA susceptibility](/preview/png/8337874.png)
چکیده انگلیسی
Addison's disease is a rare autoimmune disorder leading to adrenal insufficiency and life-long glucocorticoid dependency. Vitamin D receptor (VDR) polymorphisms and vitamin D deficiency predispose to Addison's disease. Aim of the current study was, to investigate potential anti-inflammatory vitamin D effects on monocytes in Addison's disease, focusing on inflammatory CCL-2 and IL6, as well on monocyte CD14 markers. Addison's disease is genetically linked to distinct HLA susceptibility alleles. Therefore we analyzed, whether HLA genotypes differed for vitamin D effects on monocyte markers. CD14+ monocytes were isolated from Addison's disease patients (AD, n = 13) and healthy controls (HC, n = 15) and stimulated with 1,25-dihydroxyvitamin D3 and IL1β as an inflammatory stimulant. Cells were processed for mRNA expression of CCL-2, IL6 and CD14 and DNA samples were genotyped for major histocompatibility class (MHC) class II-encoded HLA- DQA1-DQB1 haplotypes. We found a downregulation of CCL-2 after vitamin D treatment in IL1β-stimulated monocytes both from AD patients and HC (AD p < 0.001; HC p < 0.0001). CD14 expression however, was upregulated in both HC and AD patients after vitamin D treatment (p < 0.001, respectively). HC showed higher CD14 transcription level than AD patients after vitamin D treatment (p = 0.04). Compared to IL1β-induced inflammation, HC have increased CD14 levels after vitamin D treatment (p < 0.001), whereas the IL1β-induced CD14 expression of AD patients' monocytes did not change after vitamin D treatment (p = 0.8). AD patients carrying HLA high-risk haplotypes showed an increased CCL-2 expression after IL1β-induced inflammation compared to intermediate-risk HLA carriers (p = 0.05). Also HC monocytes' CD14 transcription after IL1β and vitamin D co-stimulation differed according to HLA risk profile. We show that vitamin D can exert anti-inflammatory effects on AD patients' monocytes which may be modulated by HLA risk genotypes.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The Journal of Steroid Biochemistry and Molecular Biology - Volume 177, March 2018, Pages 53-58
Journal: The Journal of Steroid Biochemistry and Molecular Biology - Volume 177, March 2018, Pages 53-58
نویسندگان
A.U. Kraus, M. Penna-Martinez, G. Meyer, K. Badenhoop,