Reduction of rat brain CD8(+) T-cells by levodopa/benserazide treatment after experimental stroke.
(2014) In European Journal of Neuroscience 40(2). p.2463-2470- Abstract
- 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... (More)
- 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)-1β, 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. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/4429664
- author
- Kuric, Enida LU and Ruscher, Karsten LU
- organization
- publishing date
- 2014
- type
- Contribution to journal
- publication status
- published
- subject
- in
- European Journal of Neuroscience
- volume
- 40
- issue
- 2
- pages
- 2463 - 2470
- publisher
- Wiley-Blackwell
- external identifiers
-
- pmid:24754803
- wos:000339716300014
- scopus:84904651469
- ISSN
- 1460-9568
- DOI
- 10.1111/ejn.12598
- language
- English
- LU publication?
- yes
- id
- 84653b51-e385-4d89-abe5-94146797e3a7 (old id 4429664)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/24754803?dopt=Abstract
- date added to LUP
- 2016-04-01 11:13:00
- date last changed
- 2022-05-06 05:19:41
@article{84653b51-e385-4d89-abe5-94146797e3a7,
abstract = {{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)-1β, 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.}},
author = {{Kuric, Enida and Ruscher, Karsten}},
issn = {{1460-9568}},
language = {{eng}},
number = {{2}},
pages = {{2463--2470}},
publisher = {{Wiley-Blackwell}},
series = {{European Journal of Neuroscience}},
title = {{Reduction of rat brain CD8(+) T-cells by levodopa/benserazide treatment after experimental stroke.}},
url = {{http://dx.doi.org/10.1111/ejn.12598}},
doi = {{10.1111/ejn.12598}},
volume = {{40}},
year = {{2014}},
}