CYTOKINE-GENE EXPRESSION IN MEASLES-INFECTED ADULT HUMAN GLIAL-CELLS

被引:42
作者
YAMABE, T
DHIR, G
COWAN, EP
WOLF, AL
BERGEY, GK
KRUMHOLZ, A
BARRY, E
HOFFMAN, PM
DHIBJALBUT, S
机构
[1] BALTIMORE VET ADM MED CTR,RETROVIRUS RES CTR,BALTIMORE,MD
[2] US FDA,CTR BIOL EVALUAT & RES,BALTIMORE,MD
[3] UNIV MARYLAND,DEPT NEUROSURG,BALTIMORE,MD
[4] UNIV MARYLAND HOSP,DEPT NEPHROL,BALTIMORE,MD 21201
关键词
MICROGLIA; INTERLEUKIN-1-BETA; INTERLEUKIN-6; TUMOR NECROSIS FACTOR ALPHA; MEASLES VIRUS;
D O I
10.1016/0165-5728(94)90193-7
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The expression of interleukin (IL)-1 beta, IL-6 and tumor necrosis factor (TNF) alpha transcripts in cultured human glial cells was examined using reverse transcription followed by polymerase chain reaction (PCR) amplification and Southern blot quantitation. Microglial cultures derived from brain biopsy specimens from three different individuals expressed transcripts for the three cytokines under basal culture conditions. This expression was enhanced in response to measles virus (MV) infection (IL-1 beta, 2.2-8.8-fold; IL-6, 2.5-8.4-fold; TNF alpha, 2.2-3.2-fold). Neither IL-1 beta nor TNF alpha transcripts were detectable in undissociated brain tissue from two individuals, suggesting that the basal expression of these cytokines in culture may have been induced by tissue dissociation or by the culture conditions. Oligodendrocytes did not express cytokine transcripts under basal culture conditions, and IL-1 beta and IL-6 but not TNF alpha transcripts could be induced by MV. Similarly, meningeal fibroblasts expressed IL-1 beta and IL-6 but not TNF alpha in response to MV-infection, suggesting that the production of TNF alpha is more cell type-restricted than either IL-1 beta or IL-6. The results indicate that adult human microglia can participate in the inflammatory response to MV infection in the CNS by producing cytokines that contribute to inflammation and demyelination. In addition, besides their role in myelination, oligodendrocytes can potentially influence immunoreactivity in the CNS by producing IL-1 beta and IL-6.
引用
收藏
页码:171 / 179
页数:9
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