Anamnestic recall of stroke-related deficits: an animal model.
Anamnestic recall of stroke-related deficits: an animal model.
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DOI：
10.1161/strokeaha.110.592865
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发表时间：
2010-11
期刊：
影响因子：
8.3
通讯作者：
Becker KJ
中科院分区：
文献类型：
--
作者：
Zierath D;Hadwin J;Savos A;Carter KT;Kunze A;Becker KJ
Anamnestic recall of stroke related deficits is a common clinical observation, especially during periods of systemic infection. The pathophysiology of this transient re-emergence of neurological dysfunction is unknown. Male Lewis rats underwent 3 hours middle cerebral artery occlusion (MCAO) and were treated with lipopolysaccharide (LPS) or saline at the time of reperfusion. The delayed type hypersensitivity (DTH) response to myelin basic protein (MBP) was examined at 28 days after MCAO. Changes in behavioral outcomes were assessed following DTH testing and repeat administration of LPS or saline at 34 days. At the time of sacrifice (36 days), the immunological response of splenocytes to MBP, neuron specific enolase (NSE) and proteolipid protein (PLP) was determined by ELISPOT assay and the number of lymphocytes in brain determined by immunocytochemistry. Animals treated with LPS at MCAO had a greater DTH response to MBP than animals treated with saline. Among those animals that had fully recovered on a given behavioral test prior to DTH testing, those treated with LPS at MCAO displayed more neurological deterioration following DTH testing and had more CD8+ lymphocytes within the ischemic core of the brain. Further, the TH1 immune response to brain antigens in spleen was more robust among those animals that deteriorated following DTH testing and there were more CD4+ lymphocytes in the penumbral region of animals with a TH1 response to MBP. Our data suggest that an immune response to brain contributes to the phenomenon of anamnestic recall of stroke related deficits following an infection. The contribution of the immune response to this phenomenon deserves further investigation.
