Platelet inhibition by low-dose acetylsalicylic acid reduces neuroinflammation in an animal model of multiple sclerosis
Please always quote using this URN: urn:nbn:de:bvb:20-opus-284535
- Aside from the established immune-mediated etiology of multiple sclerosis (MS), compelling evidence implicates platelets as important players in disease pathogenesis. Specifically, numerous studies have highlighted that activated platelets promote the central nervous system (CNS)-directed adaptive immune response early in the disease course. Platelets, therefore, present a novel opportunity for modulating the neuroinflammatory process that characterizes MS. We hypothesized that the well-known antiplatelet agent acetylsalicylic acid (ASA) couldAside from the established immune-mediated etiology of multiple sclerosis (MS), compelling evidence implicates platelets as important players in disease pathogenesis. Specifically, numerous studies have highlighted that activated platelets promote the central nervous system (CNS)-directed adaptive immune response early in the disease course. Platelets, therefore, present a novel opportunity for modulating the neuroinflammatory process that characterizes MS. We hypothesized that the well-known antiplatelet agent acetylsalicylic acid (ASA) could inhibit neuroinflammation by affecting platelets if applied at low-dose and investigated its effect during experimental autoimmune encephalomyelitis (EAE) as a model to study MS. We found that oral administration of low-dose ASA alleviates symptoms of EAE accompanied by reduced inflammatory infiltrates and less extensive demyelination. Remarkably, the percentage of CNS-infiltrated CD4\(^+\) T cells, the major drivers of neuroinflammation, was decreased to 40.98 ± 3.28% in ASA-treated mice compared to 56.11 ± 1.46% in control animals at the disease maximum as revealed by flow cytometry. More interestingly, plasma levels of thromboxane A\(_2\) were decreased, while concentrations of platelet factor 4 and glycoprotein VI were not affected by low-dose ASA treatment. Overall, we demonstrate that low-dose ASA could ameliorate the platelet-dependent neuroinflammatory response in vivo, thus indicating a potential treatment approach for MS.…
Author: | Anna Vogelsang, Susann Eichler, Niklas Huntemann, Lars Masanneck, Hannes Böhnlein, Lisa Schüngel, Alice Willison, Karin Loser, Bernhard Nieswandt, Beate E. Kehrel, Alexander Zarbock, Kerstin Göbel, Sven G. Meuth |
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URN: | urn:nbn:de:bvb:20-opus-284535 |
Document Type: | Journal article |
Faculties: | Fakultät für Biologie / Rudolf-Virchow-Zentrum |
Language: | English |
Parent Title (English): | International Journal of Molecular Sciences |
ISSN: | 1422-0067 |
Year of Completion: | 2021 |
Volume: | 22 |
Issue: | 18 |
Article Number: | 9915 |
Source: | International Journal of Molecular Sciences (2021) 22:18, 9915. https://doi.org/10.3390/ijms22189915 |
DOI: | https://doi.org/10.3390/ijms22189915 |
Dewey Decimal Classification: | 6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit |
Tag: | acetylsalicylic acid; experimental autoimmune encephalomyelitis; glycoprotein VI; multiple sclerosis; platelet factor 4; platelets; thromboxane |
Release Date: | 2023/06/29 |
Date of first Publication: | 2021/09/14 |
Licence (German): | CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International |