کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5684998 | 1597930 | 2017 | 45 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Potentiation and tolerance of toll-like receptor priming in human endothelial cells
ترجمه فارسی عنوان
پتانسیل و تحمل ابتلا به گیرنده قرص های مشابه در سلول های اندوتلیال انسان
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کلمات کلیدی
ERKIRFLTAIKKTLRIP-10hMVECHUVECTCAMYD88c-jun amino-terminal kinaseJnkIL-6LPSIκB kinase - IkB kinaseMAPK - MAPKTRIF - Trif بهlipoteichoic acid - اسید لیپتویکوئیکTIR-domain-containing adapter-inducing interferon-β - اینترفرون-β، باعث القاء آداپتور حاوی دامنه TIR می شودinterleukin 6 - اینترلوکین 6Trichostatin A - تریکوستاتین AEnzyme-linked immunosorbent assay - تست الیزاELISA - تست الیزاToll-like receptor - تیالآرhuman dermal microvascular endothelial cell - سلول اندوتلیال میکروواسکولی پوست انسانHuman umbilical vein endothelial cell - سلول اندوتلیالی ورید ناقل انسانیinterferon regulatory factor - عامل تنظیمی اینترفرونlipopolysaccharide - لیپوپلی ساکاریدpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازRIP - پاره کردنmyeloid differentiation primary response gene 88 - پاسخ اولیه ژن 88، اختلال میلوئیدinterferon gamma-induced protein 10 - پروتئین ناشی از گاما اینترفرون 10mitogen-activated protein kinase - پروتئین کیناز فعال با mitogenextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولی
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
پزشکی و دندانپزشکی (عمومی)
چکیده انگلیسی
Repeated challenge of lipopolysaccharide (LPS) alters the response to subsequent LPS exposures via modulation of toll-like receptor 4 (TLR4). Whether activation of other TLRs can modulate TLR4 responses, and vice versa, remains unclear. Specifically with regards to endothelial cells, a key component of innate immunity, the impact of TLR cross-modulation is unknown. We postulated that TLR2 priming (via Pam3Csk4) would inhibit TLR4-mediated responses while TLR3 priming (via Poly I:C) would enhance subsequent TLR4-inflammatory signaling. We studied human umbilical vein endothelial cells (HUVECs) and neonatal human dermal microvascular endothelial cells (HMVECs). Cells were primed with a combination of Poly I:C (10 μg/ml), Pam3Csk4 (10 μg/ml), or LPS (100 ng/ml), then washed and allowed to rest. They were then rechallenged with either Poly I:C, Pam3Csk4 or LPS. Endothelial cells showed significant tolerance to repeated LPS challenge. Priming with Pam3Csk4 also reduced the response to secondary LPS challenge in both cell types, despite a reduced proinflammatory response to Pam3Csk4 in HMVECs compared to HUVECs. Poly I:C priming enhanced inflammatory and interferon producing signals upon Poly I:C or LPS rechallenge, respectively. Poly I:C priming induced interferon regulatory factor 7, leading to enhancement of interferon production. Finally, both Poly I:C and LPS priming induced significant changes in receptor-interacting serine/threonine-protein kinase 1 activity. Pharmacological inhibition of receptor-interacting serine/threonine-protein kinase 1 or interferon regulatory factor 7 reduced the potentiated phenotype of TLR3 priming on TLR4 rechallenge. These results demonstrate that in human endothelial cells, prior activation of TLRs can have a significant impact on subsequent exposures and may contribute to the severity of the host response.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Translational Research - Volume 180, February 2017, Pages 53-67.e4
Journal: Translational Research - Volume 180, February 2017, Pages 53-67.e4
نویسندگان
Stephen R. Koch, Fred S. Lamb, Judith Hellman, Edward R. Sherwood, Ryan J. Stark,