QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (69) Citing Articles via Google Scholar Google Scholar Articles by Balasingam, V. Articles by Yong, V. W. Search for Related Content PubMed PubMed Citation Articles by Balasingam, V. Articles by Yong, V. W.

 Previous Article  |  Next Article 

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-

This article has been cited by other articles:

				E. MORDELET, K. KISSA, A. CRESSANT, F. GRAY, S. OZDEN, C. VIDAL, P. CHARNEAU, and S. GRANON Histopathological and cognitive defects induced by Nef in the brain FASEB J, December 1, 2004; 18(15): 1851 - 1861. [Abstract] [Full Text] [PDF]

				A. Martin, H.-D. Hofmann, and M. Kirsch Glial Reactivity in Ciliary Neurotrophic Factor-Deficient Mice after Optic Nerve Lesion J. Neurosci., July 2, 2003; 23(13): 5416 - 5424. [Abstract] [Full Text] [PDF]

				E. J. Park, S. Y. Park, E.-h. Joe, and I. Jou 15d-PGJ2 and Rosiglitazone Suppress Janus Kinase-STAT Inflammatory Signaling through Induction of Suppressor of Cytokine Signaling 1 (SOCS1) and SOCS3 in Glia J. Biol. Chem., April 18, 2003; 278(17): 14747 - 14752. [Abstract] [Full Text] [PDF]

				W. Panenka, H. Jijon, L. M. Herx, J. N. Armstrong, D. Feighan, T. Wei, V. W. Yong, R. M. Ransohoff, and B. A. MacVicar P2X7-Like Receptor Activation in Astrocytes Increases Chemokine Monocyte Chemoattractant Protein-1 Expression via Mitogen-Activated Protein Kinase J. Neurosci., September 15, 2001; 21(18): 7135 - 7142. [Abstract] [Full Text] [PDF]

				L. M. Herx, S. Rivest, and V. W. Yong Central Nervous System-Initiated Inflammation and Neurotrophism in Trauma: IL-1{beta} Is Required for the Production of Ciliary Neurotrophic Factor J. Immunol., August 15, 2000; 165(4): 2232 - 2239. [Abstract] [Full Text] [PDF]

				J. Tan, T. Town, M. Saxe, D. Paris, Y. Wu, and M. Mullan Ligation of Microglial CD40 Results in p44/42 Mitogen-Activated Protein Kinase-Dependent TNF-{alpha} Production That Is Opposed by TGF-{beta}1 and IL-10 J. Immunol., December 15, 1999; 163(12): 6614 - 6621. [Abstract] [Full Text] [PDF]

				L. Y. S. Oh, P. H. Larsen, C. A. Krekoski, D. R. Edwards, F. Donovan, Z. Werb, and V. W. Yong Matrix Metalloproteinase-9/Gelatinase B Is Required for Process Outgrowth by Oligodendrocytes J. Neurosci., October 1, 1999; 19(19): 8464 - 8475. [Abstract] [Full Text] [PDF]

				J. F. Rowell and D. E. Griffin The Inflammatory Response to Nonfatal Sindbis Virus Infection of the Nervous System Is More Severe in SJL Than in BALB/c Mice and Is Associated with Low Levels of IL-4 mRNA and High Levels of IL-10-Producing CD4+ T Cells J. Immunol., February 1, 1999; 162(3): 1624 - 1632. [Abstract] [Full Text] [PDF]

				M. Rostworowski, V. Balasingam, S. Chabot, T. Owens, and V. W. Yong Astrogliosis in the Neonatal and Adult Murine Brain Post-Trauma: Elevation of Inflammatory Cytokines and the Lack of Requirement for Endogenous Interferon-gamma J. Neurosci., May 15, 1997; 17(10): 3664 - 3674. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help