Journal
EUROPEAN JOURNAL OF NEUROSCIENCE
Volume 40, Issue 2, Pages 2463-2470Publisher
WILEY-BLACKWELL
DOI: 10.1111/ejn.12598
Keywords
cerebral ischemia; dopamine; immunomodulation; inflammation; recovery
Categories
Funding
- Swedish Research Council [2011-2684, 2011-2652]
- EU 7th workprogram through the European Stroke Network [201024]
- Hans-Christian and Alice Wachtmeister Foundation
- Swedish Brain Fund
- Thorsten och Elsa Segerfalk stiftelse
- Crafoord Foundation
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The activation of inflammatory cascades in the ischemic hemisphere impairs mechanisms of tissue reorganization with consequences for recovery of lost neurological function. Recruitment of T-cell populations to the post-ischemic brain occurs and represents a significant part of the inflammatory response. This study was conducted to investigate if treatment with levodopa, potentially acting as an immunomodulator, affects the T-cell accumulation in the post-ischemic brain. Male Sprague-Dawley rats were subjected to transient occlusion of the middle cerebral artery (tMCAO) for 105 min followed by levodopa/benserazide treatment (20 mg/kg/15 mg/kg) for 5 days initiated on day 2 post-stroke. One week after tMCAO, T-cell populations were analysed from brains, and levels of interleukin (IL)-1 beta, chemokine (C-X-C motif) ligand 1, IL-4, IL-5, interferon gamma and IL-13 were analysed. After levodopa/benserazide treatment, we found a significant reduction of cytotoxic T-cells (CD3(+)CD8(+)) in the ischemic hemisphere together with reduced levels of T-cell-associated cytokine IL-5, while other T-cell populations (CD3(+), CD3(+)CD4(+), CD3(+)CD4(+)CD25(+)) were unchanged compared with vehicle-treated rats. Moreover, a reduced number of cells was associated with reduced levels of intercellular adhesion molecule 1, expressed in endothelial cells, in the infarct core of levodopa/benserazide-treated animals. Together, we provide the first evidence that dopamine can act as a potential immunomodulator by attenuating inflammation in the post-ischemic brain.
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