MyD88-dependent toll-like receptor signaling is required for murine macrophages response to IS2

被引：9

作者：

Li, Hua ^{[1
]}

Kim, Wan-Jae ^{[1
]}

Jiang, Jun ^{[1
]}

Lee, Seung-Hwan ^{[1
]}

Youn, Hyung-Sun ^{[2
]}

Moon, Eun-Yi ^{[3
]}

Kim, Tack-Joong ^{[4
]}

Ye, Sang-Kyu ^{[5
]}

Ryu, Ji-Hwan ^{[6
]}

Kang, Tae-Bong ^{[1
]}

Koppula, Sushruta ^{[1
]}

Park, Pyo-Jam ^{[1
]}

Choi, Dong-Kug ^{[1
]}

Lee, Kwang-Ho ^{[1
]}

机构：

[1] Konkuk Univ, Coll Biomed & Hlth Sci, Dept Biotechnol, Chungju 380701, South Korea

[2] Soonchun Hyang Univ, Coll Med Sci, Dept Biomed Lab Sci, Shinchang Myun 336745, Asan Si, South Korea

[3] Sejong Univ, Dept Biosci & Biotechnol, Seoul 143747, South Korea

[4] Yonsei Univ, Div Biol Sci & Technol, Inst Biomat, Wonju 220710, South Korea

[5] Seoul Natl Univ, Coll Med, Dept Pharmacol, Seoul 110799, South Korea

[6] Yonsei Univ, Coll Med, Res Ctr Human Nat Def Syst, Seoul, South Korea

来源：

INTERNATIONAL IMMUNOPHARMACOLOGY | 2011年 / 11卷 / 10期

关键词：

beta-glucan; IS2; TLR; MyD88; MAPKs; NECROSIS-FACTOR-ALPHA; HUMAN MONOCYTIC CELLS; INNATE IMMUNE-SYSTEM; FACTOR-KAPPA-B; SACCHAROMYCES-CEREVISIAE; PATTERN-RECOGNITION; CYTOKINE PRODUCTION; CANDIDA-ALBICANS; BETA-GLUCANS; DECTIN-1;

D O I：

10.1016/j.intimp.2011.05.017

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

IS2, a soluble beta-glucan isolated from the cell wall of mutated Saccharomyces cerevisiae (S. cerevisiae) enhances the immune response compared to the wild type (WT) beta-glucan. In the present investigation we report that Toll-like receptor (TLR)/MyD88 signaling pathway was responsible in IS2 beta-glucan-mediated cellular response in RAW264.7 murine macrophages. Data revealed that IS2 beta-glucan significantly up-regulated the TLR2/TLR4 expression. Moreover. TLR2/TLR4 responds to 152 resulting in murine macrophage activation. In addition, the IS2 signal led to cytokine secretions of IL-6 and TNF-alpha. In the case of thioglycolate-elicited peritoneal macrophages from MyD88-deficient mice, the decrease in cytokines was observed. Further the mitogen-activated protein kinases (MAPKs) phosphorylation was evident and degradation of I kappa B-alpha was increased after stimulation with IS2 beta-glucan. Further examination with MyD88-deficient mice revealed that the MyD88 pathway might play an important role for IS2 beta-glucan-mediated activation of macrophages. (C) 2011 Published by Elsevier B.V

引用

页码：1578 / 1583

页数：6

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