Multiple mechanisms that prevent excessive brain inflammation.
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.
Yang
Myung-Soon
MS
Department of Pharmacology, Ajou University School of Medicine, Suwon, Kyunggi-do, Korea.
Min
Kyoung-Jin
KJ
Joe
Eunhye
E
D000818:Animals; D016207:Cytokines / Q000378:metabolism; D004660:Encephalitis / Q000276:immunology* / Q000473:pathology*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D017628:Microglia / Q000378:metabolism; D018448:Models, Immunological; D015398:Signal Transduction / Q000276:immunology*; D050826:Suppressor of Cytokine Signaling Proteins / Q000378:metabolism
D016207:Cytokines; D018836:Inflammation Mediators; D050826:Suppressor of Cytokine Signaling Proteins