TY  - JOUR
A1  - Vogelsang, Anna
A1  - Eichler, Susann
A1  - Huntemann, Niklas
A1  - Masanneck, Lars
A1  - Böhnlein, Hannes
A1  - Schüngel, Lisa
A1  - Willison, Alice
A1  - Loser, Karin
A1  - Nieswandt, Bernhard
A1  - Kehrel, Beate E.
A1  - Zarbock, Alexander
A1  - Göbel, Kerstin
A1  - Meuth, Sven G.
T1  - Platelet inhibition by low-dose acetylsalicylic acid reduces neuroinflammation in an animal model of multiple sclerosis
JF  - International Journal of Molecular Sciences
N2  - 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) 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.
KW  - acetylsalicylic acid
KW  - experimental autoimmune encephalomyelitis
KW  - platelets
KW  - multiple sclerosis
KW  - thromboxane
KW  - glycoprotein VI
KW  - platelet factor 4
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-284535
SN  - 1422-0067
VL  - 22
IS  - 18
ER  - 
TY  - JOUR
A1  - Geiger, Nina
A1  - König, Eva-Maria
A1  - Oberwinkler, Heike
A1  - Roll, Valeria
A1  - Diesendorf, Viktoria
A1  - Fähr, Sofie
A1  - Obernolte, Helena
A1  - Sewald, Katherina
A1  - Wronski, Sabine
A1  - Steinke, Maria
A1  - Bodem, Jochen
T1  - Acetylsalicylic acid and salicylic acid inhibit SARS-CoV-2 replication in precision-cut lung slices
JF  - Vaccines
N2  - Aspirin, with its active compound acetylsalicylic acid (ASA), shows antiviral activity against rhino- and influenza viruses at high concentrations. We sought to investigate whether ASA and its metabolite salicylic acid (SA) inhibit SARS-CoV-2 since it might use similar pathways to influenza viruses. The compound-treated cells were infected with SARS-CoV-2. Viral replication was analysed by RTqPCR. The compounds suppressed SARS-CoV-2 replication in cell culture cells and a patient-near replication system using human precision-cut lung slices by two orders of magnitude. While the compounds did not interfere with viral entry, it led to lower viral RNA expression after 24 h, indicating that post-entry pathways were inhibited by the compounds.
KW  - acetylsalicylic acid
KW  - salicylic acid
KW  - antiviral activity
KW  - aspirin
KW  - SARS-CoV-2
KW  - precision-cut lung slices
Y1  - 2022
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-289885
SN  - 2076-393X
VL  - 10
IS  - 10
ER  -