期刊
CYTOKINE
卷 29, 期 6, 页码 245-250出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.cyto.2004.12.002
关键词
interleukin-1; IL-1F; inflammation; signaling; CNS
资金
- Medical Research Council [G9219675] Funding Source: Medline
- Medical Research Council [G9219675] Funding Source: researchfish
- MRC [G9219675] Funding Source: UKRI
The putative new interleukin (IL)-1 family member IL-1F8 (IL-1 eta, IL-1H2) has been shown recently to activate mitogen activated protein kinases (MAPKs), extracellular signal-regulated protein kinase (ERK1/2) and c-Jun N-terminal kinase (JNK), and nuclear factor-kappa B (NF kappa B) via a mechanism that requires IL-1 Rrp2 expression in cell lines. The aim of this study was to test the hypothesis that IL-1F8 contributes to brain inflammation and injury, by studying its expression and actions in the different cell types of the mouse brain in culture. Messenger RNA for IL-1F8 was detected in neurons and glia (microglial cells, oligodendrocytes progenitor cells and to a lesser extent astrocytes) by RT-PCR. Bacterial lipopolysaccharide (LPS) had no effect on IL-1F8 mRNA levels in mixed glial cultures. Recombinant mouse IL-1 beta induced strong activation of ERK1/2, p38, JNK and NF kappa B, and significant release of IL-6 and PGE(2), which was blocked by IL-1ra. In contrast, recombinant mouse IL-1F8 did not influence any of these parameters. These results demonstrate that CNS cells may be a source of IL-1F8, but the failure of LPS to modulate IL-1F8 mRNA expression, and of recombinant IL-1F8 to induce any of the classical IL-1 responses, suggest that this cytokine has restricted activities in the brain, or that it may act via alternative pathway(s). (c) 2004 Elsevier Ltd. All rights reserved.
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