Multiple mechanisms that prevent excessive brain inflammation
- 25 July 2007
- journal article
- review article
- Published by Wiley in Journal of Neuroscience Research
- Vol. 85 (11), 2298-2305
- https://doi.org/10.1002/jnr.21254
Abstract
Inflammation of the injured brain has a double‐edged effect. Inflammation protects the brain from infection, but it aggravates injury. Furthermore, brain inflammation is considered a risk factor for neurodegenerative disorders, such as Alzheimer's and Parkinson's diseases. Emerging evidence supports the activation of negative regulatory mechanisms during this process to prevent prolonged and extensive inflammation. The inflammatory stimulators themselves or products of inflammatory cells may induce the expression of negative feedback regulators, such as suppressor of cytokine signaling (SOCS)‐family proteins, antioxidant enzymes, and antiinflammatory cytokines. Furthermore, death of activated microglia (major inflammatory cells in the brain) may regulate brain inflammation. Astrocytes, the most abundant cells in the brain, may also act in preventing microglial overactivation. Therefore, we propose that the extent and duration of brain inflammation is tightly regulated through the cooperation of multiple mechanisms to maximize antipathogenic effects and minimize tissue damage.Keywords
This publication has 108 references indexed in Scilit:
- BALT development and augmentation of hyperoxic lung injury in mice deficient in NQO1 and NQO2Free Radical Biology & Medicine, 2006
- Anti-inflammatory roles of retinoic acid in rat brain astrocytes: Suppression of interferon-γ-induced JAK/STAT phosphorylationBiochemical and Biophysical Research Communications, 2005
- Thrombin induces suppressor of cytokine signaling 3 expression in brain microglia via protein kinase Cδ activationBiochemical and Biophysical Research Communications, 2004
- Microglia expressing interleukin‐13 undergo cell death and contribute to neuronal survival in vivoGlia, 2004
- Plasminogen-induced IL-1β and TNF-α production in microglia is regulated by reactive oxygen speciesBiochemical and Biophysical Research Communications, 2003
- Interleukin‐13 and ‐4 induce death of activated microgliaGlia, 2002
- Heme oxygenase-1 mediates the anti-inflammatory effect of interleukin-10 in miceNature Medicine, 2002
- Astrocytes Modulate Nitric Oxide Production by Microglial Cells through Secretion of Serine and GlycineBiochemical and Biophysical Research Communications, 1998
- Interleukin-10 is a central regulator of the response to LPS in murine models of endotoxic shock and the Shwartzman reaction but not endotoxin tolerance.JCI Insight, 1995
- Targeted disruption of the mouse transforming growth factor-β1 gene results in multifocal inflammatory diseaseNature, 1992