ABNORMAL PRODUCTION OF INTERLEUKIN-1 BY MICROGLIA FROM TRISOMY-16 MICE

被引:19
作者
COLTON, CA
YAO, J
TAFFS, RE
KERI, JE
OSTERGRANITE, ML
机构
[1] NINCDS, BIOPHYS LAB, BETHESDA, MD 20892 USA
[2] NIAID, IMMUNOL LAB, BIOCHEM & IMMUNOPHARMACOL UNIT, BETHESDA, MD 20892 USA
[3] JOHNS HOPKINS UNIV, SCH MED, DEPT PHYSIOL, DEV GENET LAB, BALTIMORE, MD 21205 USA
[4] JOHNS HOPKINS UNIV, SCH MED, DEPT NEUROSCI, BALTIMORE, MD 21205 USA
[5] JOHNS HOPKINS UNIV, SCH MED, DEPT CELL BIOL & ANAT, BALTIMORE, MD 21205 USA
关键词
MICROGLIA; TRISOMY-16; MOUSE; DOWN SYNDROME; INTERLEUKIN-1; INTERFERON;
D O I
10.1016/0304-3940(91)90318-N
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The production of interleukin-1 (IL-1) was examined in cultured CNS microglia obtained from trisomy 16 (Ts16) fetal mouse brain, a model system for studies relevant to Down syndrome (DS). When compared to microglia from their normal littermates, Ts16 microglia produced significantly higher levels of IL-1 activity both before and following stimulation with lipopolysaccharide (LPS). IL-1 release was stimulated by alpha/beta interferon (IFN) in the normal but not Ts16 microglial cultures. The overall level of IL-1 production in normal littermates, however, was still less than that seen in Ts16. Thus, microglia from Ts16 mice may function in an inappropriate manner and, if this abnormally occurs in vivo, may have wide ranging effects on a developing nervous system.
引用
收藏
页码:270 / 274
页数:5
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