期刊
JOURNAL OF CHILD NEUROLOGY
卷 24, 期 9, 页码 1119-1126出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/0883073809338066
关键词
infection; inflammation; anti-inflammation; neuroinflammation; injury; protection; repair
资金
- NINDS NIH HHS [5R13NS040925-09, R13 NS040925] Funding Source: Medline
Preterm birth can be caused by intrauterine infection and maternal/fetal inflammatory responses. Maternal inflammation (chorioamnionitis) is often followed by a systemic fetal inflammatory response characterized by elevated levels of proinflammatory cytokines in the fetal circulation. The inflammation signal is likely transmitted across the blood-brain harrier and initiates a neuroinflammatory response. Microglial activation has a central role in this process and triggers excitotoxic, inflammatory, and oxidative damage in the developing brain. Neuroinflammation can persist over a period of time and sensitize the brain to subinjurious insults in early and chronic phases but may offer relative tolerance in the intermediate period through activation of endogenous anti-inflammatory, protective, and repair mechanisms. Neuroinflammatory injury not only destroys what exists but also changes what develops.
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