Central IL-1 differentially regulates peripheral IL-6 and TNF synthesis

被引：20

作者：

Kitamura, H

Okamoto, S

Shimamoto, Y

Morimatsu, M

Terao, A

Saito, M ^{[1
]}

机构：

[1] Hokkaido Univ, Sch Vet Med, Dept Biomed Sci, Biochem Lab, Sapporo, Hokkaido 060, Japan

[2] Hokkaido Univ, Sch Vet Med, Dept Environm Vet Med Sci, Toxicol Lab, Sapporo, Hokkaido 060, Japan

来源：

CELLULAR AND MOLECULAR LIFE SCIENCES | 1998年 / 54卷 / 03期

关键词：

interleukin-1 (IL-1); interleukin-6 (IL-6); tumour necrosis factor (TNF); autonomic nervous system; cytokine;

D O I：

10.1007/s000180050151

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Centrally given interleukin (IL)-1 is known to induce a rapid rises in blood IL-6. To extend this and to examine the mechanism by which this occurs, the effects of intracerebroventricular (icv) injection of human recombinant IL-1 beta on mRNA expression of IL-6 and tumour necrosis factor (TNF) in the spleen and liver were examined in rats. Icy injection of IL-1 produced a rapid rise of the tissue mRNA levels of IL-6 and TNF in both organs, prior to and/or in parallel with an increase in their serum levels. Pretreatment with chlorisondamine, a ganglionic blocking agent, inhibited the IL-6 responses, while it had little influence on the TNF responses. The results suggest that brain IL-1 induces peripheral production of IL-6, but not of TNF, through autonomic nervous system activation.

引用

页码：282 / 287

页数：6

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[1] THE ACUTE-PHASE RESPONSE [J].