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Volume 16, Number 9, Issue of May 1, 1996 pp. 2945-2955
Copyright ©1996 Society for Neuroscience

Attenuation of Astroglial Reactivity by Interleukin-10

Received Aug. 9, 1995; revised Feb. 13, 1996; accepted Feb. 14, 1996.

Vijayabalan Balasingam and Voon Wee Yong

Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec, Canada H3A 2B4

Prominent responses that follow brain trauma include the activation of microglia, the 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 nonreactive 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-treated 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- 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.

Key words: CNS trauma; gliosis; interleukin-10; microglia; reactive astrocytes; TNF-

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