Interleukin-10 and Interleukin-10 Receptor-I Are Upregulated in Glial Cells After an Excitotoxic Injury to the Postnatal Rat Brain

被引:55
作者
Gonzalez, Pau [1 ,2 ]
Burgaya, Ferran [5 ]
Acarin, Laia [1 ,2 ]
Peluffo, Hugo [3 ,4 ]
Castellano, Bernardo [1 ,2 ]
Gonzalez, Berta [1 ,2 ]
机构
[1] Autonomous Univ Barcelona, Dept Cellular Biol Physiol & Immunol, E-08193 Barcelona, Spain
[2] Autonomous Univ Barcelona, Inst Neurosci, E-08193 Barcelona, Spain
[3] Univ Republica, Neurodegenerat Lab, Pasteur Inst Montevideo, Montevideo, Uruguay
[4] Univ Republica, Dept Histol & Embryol, Fac Med, Montevideo, Uruguay
[5] Univ Barcelona, Dept Cell Biol, Cellular & Mol Basis Neurodegenerat & Neurorepair, Barcelona, Spain
关键词
Development; Excitotoxicity; Inflammation; Interleukin-10; receptor; Postnatal brain; CENTRAL-NERVOUS-SYSTEM; TUMOR-NECROSIS-FACTOR; HUMAN ENDOTHELIAL-CELLS; MAJOR HISTOCOMPATIBILITY COMPLEX; MESSENGER-RNA EXPRESSION; MICROGLIAL CELLS; CYTOKINE EXPRESSION; NITRIC-OXIDE; FACTOR-ALPHA; ANTIINFLAMMATORY CYTOKINES;
D O I
10.1097/NEN.0b013e31819dca30
中图分类号
R74 [神经病学与精神病学];
学科分类号
100204 [神经病学];
摘要
Inflammation is an important determinant of the severity and outcome of central nervous system injury. The endogenous anti-inflammatory cytokine interleukin-10 (IL-10) is upregulated in the injured adult central nervous system where it controls and terminates inflammatory processes. The developing brain, however, displays differences in susceptibility to insults and in associated inflammatory responses from the adult brain: the anatomic and temporal patterns of injury-induced IL-10 expression in the immature brain after excitotoxic injury are unknown. We analyzed the spaciotemporal gene and protein expression of IL-10 and its receptor (IL-10RI) in N-methyl-D-aspartate-induced excitotoxic injury in 9-day-old and control rats using quantitative reverse transcriptase polymerase chain reaction, enzyme-linked immunosorbent assay. and immunohistochemistry. Ill noninjected control brains. both molecules were expressed mainly in white matter on glial cells and blood vessels: IL-10 was also observed oil blood vessels in gray matter and in glial fibrillary acidic protein-positive processes ill the hippocampus and near leptomeningeal and ventricle surfaces. In N-methyl-D-aspartate-injected brains, IL-10 gene and protein expression,were maximal at 72 hours post-injection: IL-10RI gene and protein expression peaked at 48 hours post-injection. Interleukin-10 and IL-10RI expression in injured areas was mainly found in reactive astrocytes and in microglia/macrophages. The expression patterns of IL-10 and IL-10R suggest possible developmental roles, and their upregulation after injury Suggest,,; that this expression may have anti-inflammatory effects in distinct anatomic sites in the immature brain.
引用
收藏
页码:391 / 403
页数:13
相关论文
共 85 条
[1]
Primary cortical glial reaction versus secondary thalamic glial response in the excitotoxically injured young brain:: Microglial/macrophage response and major histocompatibility complex class I and II expression [J].
Acarin, L ;
González, B ;
Castro, AJ ;
Castellano, B .
NEUROSCIENCE, 1999, 89 (02) :549-565
[2]
Primary cortical glial reaction versus secondary thalamic glial response in the excitotoxically injured young brain:: Astroglial response and metallothionein expression [J].
Acarin, L ;
González, B ;
Hidalgo, J ;
Castro, AJ ;
Castellano, B .
NEUROSCIENCE, 1999, 92 (03) :827-839
[3]
Neuronal, astroglial and microglial cytokine expression after an excitotoxic lesion in the immature rat brain [J].
Acarin, L ;
González, B ;
Castellano, B .
EUROPEAN JOURNAL OF NEUROSCIENCE, 2000, 12 (10) :3505-3520
[4]
Acarin L, 1996, J COMP NEUROL, V367, P361
[5]
Acarin L, 2001, Prog Brain Res, V132, P375
[6]
Quantitative analysis of microglial reaction to a cortical excitotoxic lesion in the early postnatal brain [J].
Acarin, L ;
Gonzalez, B ;
Castellano, B ;
Castro, AJ .
EXPERIMENTAL NEUROLOGY, 1997, 147 (02) :410-417
[7]
Expression of inducible nitric oxide synthase and cyclooxygenase-2 after excitotoxic damage to the immature rat brain [J].
Acarin, L ;
Peluffo, H ;
González, B ;
Castellano, B .
JOURNAL OF NEUROSCIENCE RESEARCH, 2002, 68 (06) :745-754
[8]
Triflusal posttreatment inhibits glial nuclear factor-κB, downregulates the glial response, and is neuroprotective in an excitotoxic injury model in postnatal brain [J].
Acarin, L ;
González, B ;
Castellano, B .
STROKE, 2001, 32 (10) :2394-2402
[9]
Increased tumor necrosis factor and interleukin-6 production in the central nervous system of interleukin-10-deficient mice [J].
Agnello, D ;
Villa, P ;
Ghezzi, P .
BRAIN RESEARCH, 2000, 869 (1-2) :241-243
[10]
Cytokines and acute neurodegeneration [J].
Allan, SM ;
Rothwell, NJ .
NATURE REVIEWS NEUROSCIENCE, 2001, 2 (10) :734-744