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Updated: Aug 26, 2026
A Simple Approach to Induce Experimental Autoimmune Neuritis in C57BL/6 Mice for Functional and Neuropathological Assessments
Published on: November 9, 2017
Deficient p75 low-affinity neurotrophin receptor expression exacerbates experimental allergic encephalomyelitis in
Sjef Copray1, Britta Küst, Bart Emmer
1Department of Medical Physiology, University of Groningen, A.Deusinglaan 1, 9713 AV Groningen KZ, Netherlands. j.c.v.m.copray@med.rug.nl
Abstract:
We have investigated the role of p75NTR in inflammation in experimental allergic encephalomyelitis (EAE), a model for the human disease multiple sclerosis (MS). Induction of EAE in C57/BL6 wild-type mice resulted in expression of p75NTR in endothelial cells in the CNS. In contrast to the clinical manifestation of EAE observed in wild-type C57/BL6 mice, mice deficient for p75NTR (p75NTR knockout mice) developed severe or lethal disease and concomitant increased levels of inflammation in the CNS. Our findings suggest a physiological significant role for p75NTR in CNS endothelial cells during inflammation and involvement in preservation of blood-brain barrier integrity during a severe infiltrative attack.
Insights
The p75 neurotrophin receptor (p75NTR) plays a protective role in central nervous system (CNS) inflammation. Its absence exacerbates experimental allergic encephalomyelitis (EAE), a multiple sclerosis model, highlighting p75NTR
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS).
- The p75 neurotrophin receptor (p75NTR) is implicated in various cellular processes, including inflammation.
- Experimental allergic encephalomyelitis (EAE) serves as a key animal model for studying MS pathogenesis.
Purpose of the Study:
- To investigate the role of p75NTR in the inflammatory processes of EAE.
- To determine the impact of p75NTR deficiency on disease severity and CNS inflammation in an MS model.
Main Methods:
- Induction of EAE in wild-type and p75NTR knockout mice.
- Analysis of p75NTR expression in CNS endothelial cells during EAE.
- Assessment of clinical disease manifestations and CNS inflammation levels.
Main Results:
- p75NTR was expressed in CNS endothelial cells upon EAE induction in wild-type mice.
- p75NTR knockout mice exhibited significantly more severe or lethal EAE.
- Absence of p75NTR correlated with increased CNS inflammation levels.
Conclusions:
- p75NTR has a significant physiological role in CNS endothelial cells during inflammation.
- p75NTR is involved in maintaining blood-brain barrier integrity during severe inflammatory attacks in EAE.
- Targeting p75NTR may offer therapeutic potential for MS and other CNS inflammatory conditions.
