Related Experiment Video
Updated: Oct 21, 2025
Myelin Oligodendrocyte Glycoprotein MOG35-55 Induced Experimental Autoimmune Encephalomyelitis EAE in C57BL/6 Mice
Published on: April 15, 2014
Eosinophils are dispensable for development of MOG35-55-induced experimental autoimmune encephalomyelitis in mice
Klara Ruppova1, Jong-Hyung Lim1, Georgia Fodelianaki1
1Institute for Clinical Chemistry and Laboratory Medicine, University Clinic, Technische Universität Dresden, Dresden, Germany.
Abstract:
Experimental autoimmune encephalomyelitis (EAE) represents the mouse model of multiple sclerosis, a devastating neurological disorder. EAE development and progression involves the infiltration of different immune cells into the brain and spinal cord. However, less is known about a potential role of eosinophil granulocytes for EAE disease pathogenesis. In the present study, we found enhanced eosinophil abundance accompanied by increased concentration of the eosinophil chemoattractant eotaxin-1 in the spinal cord in the course of EAE induced in C57BL/6 mice by immunization with MOG35-55 peptide. However, the absence of eosinophils did not affect neuroinflammation, demyelination and clinical development or severity of EAE, as assessed in ∆dblGATA1 eosinophil-deficient mice. Taken together, despite their enhanced abundance in the inflamed spinal cord during disease progression, eosinophils were dispensable for EAE development.
Insights
In experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis, eosinophils accumulate in the spinal cord. However, these eosinophils are not essential for EAE development or severity.
Area of Science:
- Neuroimmunology
- Immunology
- Pathology
Background:
- Experimental autoimmune encephalomyelitis (EAE) is a widely used mouse model for multiple sclerosis (MS).
- Immune cell infiltration into the central nervous system (CNS) is a hallmark of EAE pathogenesis.
- The specific role of eosinophil granulocytes in EAE remains poorly understood.
Purpose of the Study:
- To investigate the role of eosinophils in the pathogenesis of MOG35-55 peptide-induced EAE in C57BL/6 mice.
- To determine if eosinophil absence impacts neuroinflammation, demyelination, and clinical disease progression in EAE.
Main Methods:
- Induction of EAE in C57BL/6 mice using MOG35-55 peptide immunization.
- Assessment of eosinophil abundance and eotaxin-1 concentration in the spinal cord during EAE.
- Evaluation of EAE in eosinophil-deficient (∆dblGATA1) mice compared to wild-type controls.
Main Results:
- EAE induction led to increased eosinophil infiltration and elevated eotaxin-1 levels in the spinal cord.
- Absence of eosinophils in ∆dblGATA1 mice did not alter the extent of neuroinflammation.
- Demyelination and clinical EAE severity were unaffected in eosinophil-deficient mice.
Conclusions:
- Eosinophils are recruited to the spinal cord during EAE.
- Despite their presence, eosinophils are dispensable for the development and progression of EAE.
- These findings suggest that other immune cells play a dominant role in EAE pathogenesis.
More Related Videos
08:47Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
Published on: May 8, 2016
10:47Simple and Efficient Production and Purification of Mouse Myelin Oligodendrocyte Glycoprotein for Experimental Autoimmune Encephalomyelitis Studies
Published on: October 27, 2016