期刊
JOURNAL OF NEUROIMMUNOLOGY
卷 153, 期 1-2, 页码 50-63出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2004.04.013
关键词
TLR9; CpG ODN; astrocytes; JNK; NF-kappa B
资金
- NIAID NIH HHS [AI43477] Funding Source: Medline
- NIEHS NIH HHS [ES06376] Funding Source: Medline
Bacterial DNA and synthetic oligodeoxynucleotides (ODN) containing unmethylated CpG motifs stimulate the cells of the innate immune system through a specific receptor called Toll-like receptor-9 (TLR9). It was reported that CpG ODN stimulation induces activation of astrocytes and microglia. However, the precise intracellular signaling pathways that lead to this glial cell activation have not been clearly elucidated. In this study, we found that CpG ODN induce mRNA expression of adhesion molecules and matrix metalloproteinase-9 (MMP-9), as well as proinflammatory cytokines and chemokines, in mouse astrocytes. CpG ODN stimulation in astrocytes induces the activation of IkappaB kinase (IKK) and c-Jun N-terminal kinase (INK), whereas it inhibits the constitutive ERK1/2 activation. The abrogation of JNK activity using a pharmacological inhibitor showed that INK activation is essential for the induction of cytokine and chemokine gene expression. This effect of INK does not require the phosphorylation of c-Jun; rather, it works via the potentiation of NF-kappaB signaling. (C) 2004 Elsevier B.V. All rights reserved.
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