The role of inflammation in perinatal brain injury

被引：0

作者：

Henrik Hagberg

Carina Mallard

Donna M. Ferriero

Susan J. Vannucci

Steven W. Levison

Zinaida S. Vexler

Pierre Gressens

机构：

[1] Centre for the Developing Brain,Division of Imaging Sciences and Biomedical Engineering

[2] King's College London,Departments of Neurology and Pediatrics

[3] King's Health Partners,Department of Pediatrics/Newborn Medicine

[4] St Thomas' Hospital,Department of Neurology and Neuroscience

[5] Perinatal Center,undefined

[6] Institute of Physiology and Neurosciences and Clinical Sciences,undefined

[7] Sahlgrenska Academy,undefined

[8] University of Gothenburg,undefined

[9] University of California San Francisco,undefined

[10] Weill Cornell Medical College,undefined

[11] Rutgers University,undefined

[12] RBHS–New Jersey Medical School,undefined

[13] Cancer Center,undefined

[14] Inserm,undefined

[15] U1141,undefined

来源：

Nature Reviews Neurology | 2015年 / 11卷

关键词：

D O I：

暂无

中图分类号：

学科分类号：

摘要：

Perinatal brain injuries result from a spectrum of conditions, including neonatal encephalopathy, arterial ischaemic stroke, prematurity, and systemic infectionsDepending on the timing and context, inflammation can prime the brain for injury or exert protective actionsPattern recognition receptors, such as Toll-like receptors on innate immune cells (microglia, mast cells and macrophages), are important participants in the early phases of injury, and can increase CNS vulnerability (sensitization)Inflammation during preterm labour and intensive care of premature infants affects the very immature brain during critical phases of brain development, with serious consequences for myelination and cortical developmentUnderstanding the involvement of inflammation in perinatal brain injury can aid identification of new strategies for prevention and treatment that could reduce neurological and neuropsychiatric morbidities in maturing infants

引用

页码：192 / 208

页数：16

共 402 条

[1]

Galea I(2007)What is immune privilege (not)? Trends Immunol. 28 12-18

[2]

Bechmann I(2011)Schizophrenia and autism: both shared and disorder-specific pathogenesis via perinatal inflammation? Pediatr. Res. 69 26R-33R

[3]

Perry VH(2012)Inflammation during fetal and neonatal life: implications for neurologic and neuropsychiatric disease in children and adults Ann. Neurol. 71 444-457

[4]

Meyer U(2014)Mechanisms of perinatal arterial ischemic stroke J. Cereb. Blood Flow Metab. 34 921-932

[5]

Feldon J(2010)The role of pattern-recognition receptors in innate immunity: update on Toll-like receptors Nat. Immunol. 11 373-384

[6]

Dammann O(2010)Sterile inflammation: sensing and reacting to damage Nat. Rev. Immunol. 10 826-837

[7]

Hagberg H(2011)Regulation of Toll-like receptor 1 and -2 in neonatal mice brains after hypoxia–ischemia J. Neuroinflammation 8 45-227

[8]

Gressens P(2013)Regulation of Toll-like receptors in the choroid plexus in the immature brain after systemic inflammatory stimuli Transl. Stroke Res. 4 220-13984

[9]

Mallard C(2008)Toll-like receptor 3 is a negative regulator of embryonic neural progenitor cell proliferation J. Neurosci. 28 13978-215

[10]

Fernandez–Lopez D(2006)Toll-like receptor 8 functions as a negative regulator of neurite outgrowth and inducer of neuronal apoptosis J. Cell Biol. 175 209-139

← 1 2 3 4 5 6 7 8 9 10 →