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

[41]

Hsiao EY(2008)Mast cell stabilization limits hypoxic–ischemic brain damage in the immature rat Brain Pathol. 18 1-218

[42]

Patterson PH(2014)Stroke induces histamine accumulation and mast cell degranulation in the neonatal rat brain EMBO J. 33 7-1805

[43]

McAllister AK(2013)The resolution of neuroinflammation in neurodegeneration: leukocyte recruitment via the choroid plexus Nat. Rev. Immunol. 13 206-808

[44]

Stolp HB(2007)Orchestrated leukocyte recruitment to immune-privileged sites: absolute barriers versus educational gates J. Cereb. Blood Flow Metab. 27 1798-309

[45]

Nathan C(2011)T- and B-cell-deficient mice with experimental stroke have reduced lesion size and inflammation Nat. Med. 17 796-308

[46]

McRae A(2009)The immunology of stroke: from mechanisms to translation J. Immunol. 183 298-871

[47]

Gilland E(2010)Early life exposure to lipopolysaccharide suppresses experimental autoimmune encephalomyelitis by promoting tolerogenic dendritic cells and regulatory T cells Biochem. Biophys. Res. Commun. 398 302-20106

[48]

Bona E(2011)Neonatal endotoxin exposure suppresses experimental autoimmune encephalomyelitis through regulating the immune cells responsivity in the central nervous system of adult rats Brain Behav. Immun. 25 863-1106

[49]

Hagberg H(2006)Maternal immune stimulation during pregnancy affects adaptive immunity in offspring to promote development of TH17 cells J. Biol. Chem. 281 20095-2486

[50]

Jin Y(2001)MEK–ERK signaling is involved in interferon-γ-induced death of oligodendroglial progenitor cells Eur. J. Neurosci. 13 1101-341

← 1 2 3 4 5 6 7 8 9 10 →