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Selenium suppresses the activation of transcription factor NF-kappa B and IRF3 induced by TLR3 or TLR4 agonists

Authors
Youn, Hyung-SunLim, Hyo JinChoi, Yong JoonLee, Joo YoungLee, Mi-YoungRyu, Jae-Ha
Issue Date
Mar-2008
Publisher
ELSEVIER SCIENCE BV
Keywords
toll like receptors; selenium; interferon regulatory factor 1
Citation
INTERNATIONAL IMMUNOPHARMACOLOGY, v.8, no.3, pp.495 - 501
Journal Title
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume
8
Number
3
Start Page
495
End Page
501
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/14316
DOI
10.1016/j.intimp.2007.12.008
ISSN
1567-5769
Abstract
Toll-like receptors (TLRs) play an important role in recognition of microbial components and induce innate immune responses by recognizing invading microbial pathogens leading to the activation of the adaptive immune responses. The microbial components trigger the activation of two downstream signaling pathways of TLRs; MyD88- and TRIF-dependent pathways leading to the expression of pro-inflammatory cytokines and type I interferons (IFNs). The MyD88- and TRIF-dependent pathways lead to the activation of NF-kappa B and IRF3 through the activation of IKK-beta and TBK1, respectively. Selenium is an essential trace element nutrient possessing anticarcinogenic properties. Here, we attempted to identify the molecular targets of selenium in TLR signaling pathways. Selenium inhibited NF-kappa B activation induced by poly[I:C] (TLR3 agonist), LIPS (TLR4 agonist) or overexpression of MyD88 or IKK-beta which is the key kinase of MyD88-dependent signaling pathway. Selenium inhibited IRF3 activation induced by poly[I:C], LPS or the overexpression of TRIF or TBK1. Selenium also suppressed the expression of COX-2 and iNOS and the endogenous IFN beta mRNA induced by poly[I:C] or LIPS. Therefore, our results suggest that selenium can modulate both MyD88- and TRIF-dependent signaling pathways of TLRs leading to decreased inflammatory gene expression. (c) 2008 Elsevier B.V. All rights reserved.
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