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Multiple mechanisms that prevent excessive brain inflammation.

Authors
Yang, MS; Min, KJ; Joe, E
Citation
Journal of neuroscience research, 85(11):2298-2305, 2007
Journal Title
Journal of neuroscience research
ISSN
0360-40121097-4547
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.
MeSH terms
AnimalsCytokines/metabolismEncephalitis/immunology*Encephalitis/pathology*HumansInflammation Mediators/metabolism*Microglia/metabolismModels, Immunological*Signal Transduction/immunology*Suppressor of Cytokine Signaling Proteins/metabolism
DOI
10.1002/jnr.21254
PMID
17348044
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
AJOU Authors
조, 은혜
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