Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
The myelin sheath surrounding axons is vulnerable to mechanical stresses after head injuries, as well as autoimmune attacks and degeneration in neurological disorders. Unfortunately, there is currently no effective method to assess these axonal conditions in individual patients. We have developed a sandwich immunoassay detecting dual signals of myelin oligodendrocyte glycoprotein (MOG) and interleukin 1B (IL1B) in human plasma ([IL1B on MOG]). While IL1B is one of common inflammation markers, its lack of tissue specificity is addressed by identifying IL1B on extracellular vesicles from oligodendrocytes isolated using anti-MOG, suggesting inflammation around axons. In 77 control subjects, plasma levels of [IL1B on MOG] did not increase more than 2 fold from baseline. During the sports season, 14% (151 football players) and 22% (18 rugby players) exhibited a substantial 2-17 fold increase, despite the absence of traumatic brain injuries. This elevation demonstrated a non-random pattern, with some individuals gradually rising towards the season's end, followed by a decline. [IL1B on MOG] levels also correlated with the clinical course of a post-concussion syndrome case. These data indicate that [IL1B on MOG] blood test is a potential marker for assessing mild axonal neuroinflammation.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10980150 | PMC |
| http://dx.doi.org/10.21203/rs.3.rs-3997676/v1 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The myelin sheath surrounding axons is vulnerable to mechanical stresses after head injuries, as well as autoimmune attacks and degeneration in neurological disorders. Unfortunately, there is currently no effective method to assess these axonal conditions in individual patients. We have developed a sandwich immunoassay detecting dual signals of myelin oligodendrocyte glycoprotein (MOG) and interleukin 1B (IL1B) in human plasma ([IL1B on MOG]).
View Article and Find Full Text PDFThe C-type lectin receptor Clec1A plays an important role in the development of experimental autoimmune encephalomyelitis by enhancing antigen presenting ability of dendritic cells and inducing inflammatory cytokine IL-17.
Exp Anim
August 2022
Center for Animal Disease Models, Research Institute for Biomedical Sciences, Tokyo University of Science, 2669 Yamazaki, Noda, Chiba 278-0022, Japan.
Clec1A, a member of C-type lectin receptor family, has a carbohydrate recognition domain in its extracellular region, but no known signaling motif in the cytoplasmic domain. Clec1a is highly expressed in endothelial cells and weakly in dendritic cells. Although this molecule was reported to play an important role in the host defense against Aspergillus fumigatus by recognizing 1,8-dihydroxynaphthalene-melanin on the fungal surface, the roles of this molecule in un-infected animals remain to be elucidated.
View Article and Find Full Text PDFDeletion of inflammasome adaptor protein ASC enhances functional recovery after spinal cord injury in mice.
J Orthop Sci
May 2021
Department of Orthopaedics, Jichi Medical University School of Medicine, Tochigi, 329-0498, Japan.
Background: Research has revealed the crucial roles of inflammasomes in various central nervous system disorders. However, the role of inflammasomes in secondary damage following spinal cord injury (SCI) remains incompletely understood.
Methods: Here, we investigated the role of apoptosis-associated speck-like protein (ASC), an adaptor protein for inflammasome formation, after contusion SCI in ASC homozygous knockout (ASC) mice.
Neutrophil-selective deletion of Cxcr2 protects against CNS neurodegeneration in a mouse model of multiple sclerosis.
J Neuroinflammation
February 2020
Department of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA.
Background: Multiple sclerosis (MS) is a chronic debilitating immune-mediated disease of the central nervous system (CNS) driven by demyelination and gray matter neurodegeneration. We previously reported an experimental autoimmune encephalomyelitis (EAE) MS mouse model with elevated serum CXCL1 that developed severe and prolonged neuron damage. Our findings suggested that CXCR2 signaling may be important in neuronal damage, thus implicating neutrophils, which express CXCR2 in abundance, as a potential cell type involved.
View Article and Find Full Text PDFPhysical Exercise Attenuates Experimental Autoimmune Encephalomyelitis by Inhibiting Peripheral Immune Response and Blood-Brain Barrier Disruption.
Mol Neurobiol
August 2017
Laboratory of Autoimmunity and Immunopharmacology, Campus Araranguá, Universidade Federal de Santa Catarina, Rodovia Jorge Lacerda, Km 35,4-Jardim das Avenidas, 88900-000, Araranguá, SC, Brazil.
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) caused by demyelination, immune cell infiltration, and axonal damage. Herein, we sought to investigate the influence of physical exercise on mice experimental autoimmune encephalomyelitis (EAE), a reported MS model. Data show that both strength and endurance training protocols consistently prevented clinical signs of EAE and decreased oxidative stress, an effect which was likely due to improving genomic antioxidant defense-nuclear factor erythroid 2-related factor (Nrf2)/antioxidant response elements (ARE) pathway-in the CNS.
View Article and Find Full Text PDF