Procyanidin dimer B2-mediated IRAK-M induction negatively regulates TLR4 signaling in macrophages
- Authors
- Sung, Nak-Yun; Yang, Mi-So; Song, Du-Sub; Kim, Jae-Kyung; Park, Jong-Heum; Song, Beom-Seok; Park, Sang-Hyun; Lee, Ju-Woon; Park, Hyun-Jin; Kim, Jae-Hun; Byun, Eui-Baek; Byun, Eui-Hong
- Issue Date
- 16-8월-2013
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Procyanidin B2; Toll-like receptor; Cytokine; Mitogen-activated protein kinases; Nuclear factor kappa B
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.438, no.1, pp.122 - 128
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 438
- Number
- 1
- Start Page
- 122
- End Page
- 128
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/102440
- DOI
- 10.1016/j.bbrc.2013.07.038
- ISSN
- 0006-291X
- Abstract
- Polyphenolic compounds have been found to possess a wide range of physiological activities that may contribute to their beneficial effects against inflammation-related diseases; however, the molecular mechanisms underlying this anti-inflammatory activity are not completely characterized, and many features remain to be elucidated. In this study, we investigated the molecular basis for the down-regulation of toll-like receptor 4 (TLR4) signal transduction by procyanidin dimer 82 (Pro 82) in macrophages. Pro B2 markedly elevated the expression of the interleukin (IL)-1 receptor-associated kinase (IRAK)-M protein, a negative regulator of TLR signaling. Lipopolysaccharide (LPS)-induced expression of cell surface molecules (CD80, CD86, and MHC class I/II) and production of pro-inflammatory cytokines (tumor necrosis factor-alpha, IL-1 beta, IL-6, and IL-12p70) were inhibited by Pro B2, and this action was prevented by IRAK-M silencing. In addition, Pro B2-treated macrophages inhibited LPS-induced activation of mitogen-activated protein kinases such as extracellular signal-regulated kinase 1/2, p38, and c-Jun N-terminal kinase and the translocation of nuclear factor kappa B and p65 through IRAK-M. We also found that Pro B2-treated macrophages inactivated naive T cells by inhibiting LPS-induced interferon-gamma and IL-2 secretion through IRAK-M. These novel findings provide new insights into the understanding of negative regulatory mechanisms of the TLR4 signaling pathway and the immune-pharmacological role of Pro 82 in the immune response against the development and progression of many chronic diseases. (C) 2013 Elsevier Inc. All rights reserved.
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Collections - Graduate School > Department of Biotechnology > 1. Journal Articles
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