Czech, Bozena; Pfeilschifter, Waltraud; Mazaheri-Omrani, Niloufar; Strobel, Marc André; Kahles, Timo; Neumann-Haefelin, Tobias; Rami, Abdelhaq; Huwiler, Andrea; Pfeilschifter, Josef (2009). The immunomodulatory sphingosine 1-phosphate analog FTY720 reduces lesion size and improves neurological outcome in a mouse model of cerebral ischemia. Biochemical and biophysical research communications, 389(2), pp. 251-6. Orlando, Fla.: Academic Press 10.1016/j.bbrc.2009.08.142
Full text not available from this repository.Cerebral ischemia is accompanied by fulminant cellular and humoral inflammatory changes in the brain which contribute to lesion development after stroke. A tight interplay between the brain and the peripheral immune system leads to a biphasic immune response to stroke consisting of an early activation of peripheral immune cells with massive production of proinflammatory cytokines followed by a systemic immunosuppression within days of cerebral ischemia that is characterized by massive immune cell loss in spleen and thymus. Recent work has documented the importance of T lymphocytes in the early exacerbation of ischemic injury. The lipid signaling mediator sphingosine 1-phosphate-derived stable analog FTY720 (fingolimod) acts as an immunosuppressant and induces lymphopenia by preventing the egress of lymphocytes, especially T cells, from lymph nodes. We found that treatment with FTY720 (1mg/kg) reduced lesion size and improved neurological function after experimental stroke in mice, decreased the numbers of infiltrating neutrophils, activated microglia/macrophages in the ischemic lesion and reduced immunohistochemical features of apoptotic cell death in the lesion.
Item Type: |
Journal Article (Original Article) |
|---|---|
Division/Institute: |
04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Pharmacology |
UniBE Contributor: |
Huwiler, Andrea |
ISSN: |
0006-291X |
Publisher: |
Academic Press |
Language: |
English |
Submitter: |
Factscience Import |
Date Deposited: |
04 Oct 2013 15:10 |
Last Modified: |
05 Dec 2022 14:21 |
Publisher DOI: |
10.1016/j.bbrc.2009.08.142 |
PubMed ID: |
19720050 |
Web of Science ID: |
000270764400009 |
URI: |
https://boris.unibe.ch/id/eprint/30672 (FactScience: 194936) |
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