Quantum dots induced interferon beta expression via TRIF-dependent signaling pathways by promoting endocytosis of TLR4

被引：14
作者：
Ho, Chia-Chi [1 ]
Luo, Yueh-Hsia [1 ]
Chuang, Tsung-Hsien [2 ]
Lin, Pinpin [1 ]
机构：
[1] Natl Hlth Res Inst, Natl Inst Environm Hlth Sci, Zhunan, Taiwan
[2] Natl Hlth Res Inst, Immunol Res Ctr, Zhunan, Taiwan
来源：
TOXICOLOGY | 2016年 / 344卷
关键词：
QD705; Inflammation; IFN-beta; TRIF; TLR4; TOLL-LIKE-RECEPTORS; NF-KAPPA-B; TITANIUM-DIOXIDE NANOPARTICLES; ADAPTIVE IMMUNE-RESPONSES; IFN-REGULATORY FACTOR-3; WALL CARBON NANOTUBES; TRANSCRIPTION FACTORS; INDEPENDENT PATHWAYS; PULMONARY TOXICITY; UP-REGULATION;
D O I：
10.1016/j.tox.2016.02.005
中图分类号：
R9 [药学];
学科分类号：
1007 ;
摘要：
Quantum dots (QDs) are nano-sized semiconductors. Previously, intratracheal instillation of QD705s induces persistent inflammation and remodeling in the mouse lung. Expression of interferon beta (IFN-beta), involved in tissue remodeling, was induced in the mouse lung. The objective of this study was to understand the mechanism of QD705 induced interferon beta (IFN-beta) expression. QD705-COOH and QD705-PEG increased IFN-beta and IP-10 mRNA levels during day1 to 90 post-exposure in mouse lungs. QD705-COOH increased IFN-beta expression via Toll/interleukin-1 receptor domain-containing adapter protein (TRIF) dependent Toll-like receptor (TLR) signaling pathways in macrophages RAW264.7. Silencing TRIF expression with siRNA or co-treatment with a TRIF inhibitor tremendously abolished QD705s-induced IFN-beta expression. Co-treatment with a TLR4 inhibitor completely prevented IFN-beta induction by QD705-COOH. QD705-COOH readily entered cells, and co-treatment with either inhibitors of endocytosis or intracellular TLRs prevented IFN-beta induction. Thus, activation of the TRIF dependent TLRs pathway by promoting endocytosis of TLR4 is one of the mechanisms for immunomodulatory effects of nanoparticles. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码：61 / 70
页数：10
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