PMID- 8622125
OWN - NLM
STAT- MEDLINE
DCOM- 19960618
LR  - 20211109
IS  - 0270-6474 (Print)
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Linking)
VI  - 16
IP  - 9
DP  - 1996 May 1
TI  - Attenuation of astroglial reactivity by interleukin-10.
PG  - 2945-55
AB  - Prominent responses that follow brain trauma include the activation of microglia, 
      recruitment of blood-derived macrophages, and astroglial reactivity. Based on 
      evidence that cytokines produced by macrophages/microglia may cause astrocytes to 
      become reactive, the aim of this study was to determine whether astroglial 
      reactivity could be attenuated by interleukin (IL)-10, a potent inhibitor of 
      cytokine synthesis by macrophages/microglia. Four days after the local 
      application of IL-10 to the site of corticectomy in adult mice, the number of 
      reactive astrocytes and their state of hypertrophy was reduced (by 60%) when 
      compared with vehicle controls. In the majority of IL-10-treated mice, but not in 
      any vehicle controls, the tissue in the immediate vicinity of IL-10 application 
      contained viable but non reactive astrocytes. The mechanism by which IL-10 
      attenuates astroglial reactivity is likely via the reduction of cytokine 
      production by macrophages/microglia because, based on Mac-1 immunohistochemistry, 
      the macrophages/microglia of IL-10 brains had a decreased activation state 
      compared with vehicle-controls. Another macrophage/microglia deactivating agent, 
      macrophage inhibitory factor, also reduced astroglial activity in vivo. 
      Furthermore, IL-10 had no direct effect on purified astrocytes in culture, 
      indicating that its in vivo action on astroglial reactivity is likely via 
      indirect mechanisms. Finally, injury resulted in the substantial rise of tumor 
      necrosis factor-alpha mRNA levels, and this elevation was significantly inhibited 
      by IL-10. The ability to manipulate the extent of astrogliosis should provide a 
      means of addressing the neurotrophic or inhibitory role of reactive astrocytes in 
      neurological recovery.
FAU - Balasingam, V
AU  - Balasingam V
AD  - Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill 
      University, Quebec, Canada.
FAU - Yong, V W
AU  - Yong VW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Macrophage Migration-Inhibitory Factors)
RN  - 0 (Macrophage-1 Antigen)
RN  - 0 (Oligonucleotide Probes)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 130068-27-8 (Interleukin-10)
SB  - IM
MH  - Animals
MH  - Astrocytes/*drug effects/pathology/physiology
MH  - Base Sequence
MH  - Female
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - Gliosis/pathology
MH  - Immunohistochemistry
MH  - Interleukin-10/*pharmacology
MH  - Macrophage Migration-Inhibitory Factors/metabolism
MH  - Macrophage-1 Antigen/metabolism
MH  - Mice
MH  - Molecular Sequence Data
MH  - Oligonucleotide Probes/genetics
MH  - Polymerase Chain Reaction
MH  - RNA, Messenger/metabolism
MH  - Transcription, Genetic
MH  - Tumor Necrosis Factor-alpha/genetics
PMC - PMC6579053
EDAT- 1996/05/01 00:00
MHDA- 1996/05/01 00:01
PMCR- 1996/11/01
CRDT- 1996/05/01 00:00
PHST- 1996/05/01 00:00 [pubmed]
PHST- 1996/05/01 00:01 [medline]
PHST- 1996/05/01 00:00 [entrez]
PHST- 1996/11/01 00:00 [pmc-release]
AID - 10.1523/JNEUROSCI.16-09-02945.1996 [doi]
PST - ppublish
SO  - J Neurosci. 1996 May 1;16(9):2945-55. doi: 10.1523/JNEUROSCI.16-09-02945.1996.