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Author Spotlight: Creating a Versatile Experimental Autoimmune Encephalomyelitis Model Relevant for Both Male and Female Mice
Published on: October 13, 2023
Characterization of leptomeningeal inflammation in rodent experimental autoimmune encephalomyelitis (EAE) model of
Suyog Pol1, Ferdinand Schweser2, Nicola Bertolino1
1Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA.
Background:
Leptomeningeal inflammation, as evidenced by leptomeningeal contrast enhancement (LMCE), is associated to cortical pathology in multiple sclerosis. The temporal pattern of LMCE in experimental autoimmune encephalomyelitis (EAE) myelin oligodendrocyte glycoprotein (MOG) is unknown.
Objective:
To investigate LMCE using serial MRI in the EAE model of MS, and its association with clinical disease progression. To characterize the relationship between LMCE and underlying histological correlates.
Design:
Thirteen C57BL/6J mice, MOG-immunized (35-55 amino acid) and 8 saline injected animals were assessed at pre-induction and at 3, 6, 10, 20, 27, 32, 45 and 63 days post induction (dPI). LMCE scan was obtained using FLAIR-RARE sequence after post-contrast gadolinium administration on 9.4 T scanner. Brain cryo-sections were assessed for measuring cellular density of Iba1 positive macrophage/microglia at 10 dPI and 32 dPI, and for the presence of T, B and macrophage cells in the meningeal layer at 10 dPI and 63 dPI.
Results:
All EAE-MOG animals showed presence of LMCE and none of the control mice. The peak signal intensity of LMCE was evidenced at 10dPI in the meninges and decreased through 10-63 dPI. The peak of LMCE was associated with a weight loss starting at 1 week PI and with clinical symptoms starting at 2 weeks PI. Histological analysis of the brain tissue showed a higher density of Iba1 positive microglial cells in the EAE-MOG animals, corresponding to the areas of LMCE. Meninges of EAE mice showed higher density of Iba1 stained macrophage cells relative to saline animals. EAE animals also showed the presence of T and B cells in the meninges which were absent in the saline animals.
Conclusions:
LMCE peak intensity in the meninges corresponds to the acute inflammatory phase of EAE-MOG disease progression, and is associated with clinical symptoms and higher inflammatory cell density.
Insights
Leptomeningeal contrast enhancement (LMCE) peaks early in experimental autoimmune encephalomyelitis (EAE) mouse models, correlating with disease severity. This imaging marker reflects acute inflammation and is linked to clinical symptoms and increased immune cell presence in the meninges.
Area of Science:
- Neuroimmunology
- Neuroinflammation
- Medical Imaging
Background:
- Leptomeningeal inflammation, indicated by leptomeningeal contrast enhancement (LMCE), is linked to cortical pathology in multiple sclerosis (MS).
- The temporal dynamics of LMCE in the myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) model of MS remain uncharacterized.
Purpose of the Study:
- To investigate the temporal pattern of LMCE using serial MRI in the EAE model of MS.
- To assess the association between LMCE and clinical disease progression.
- To characterize the relationship between LMCE and underlying histological findings.
Main Methods:
- Thirteen C57BL/6J mice immunized with MOG (35-55 amino acid) and 8 saline-injected controls underwent serial MRI (9.4 T) with gadolinium contrast.
- LMCE was assessed using a FLAIR-RARE sequence at multiple time points post-induction (3-63 days).
- Brain cryo-sections were analyzed for Iba1-positive microglia/macrophages and meningeal T, B, and macrophage cells at 10 and 32 days post-induction.
Main Results:
- All EAE-MOG mice exhibited LMCE, while control mice did not.
- Peak LMCE signal intensity occurred at 10 days post-induction (dPI) and decreased between 10-63 dPI.
- Peak LMCE correlated with weight loss starting at 1 week post-induction and clinical symptoms appearing at 2 weeks post-induction.
- Histological analysis revealed increased Iba1-positive microglia/macrophages in EAE-MOG mice, corresponding to LMCE areas.
- EAE mice showed increased meningeal macrophages, T cells, and B cells compared to controls.
Conclusions:
- The peak intensity of LMCE in the meninges aligns with the acute inflammatory phase of EAE-MOG.
- LMCE is associated with clinical symptoms and increased inflammatory cell density in this MS model.
- LMCE serves as a valuable imaging marker for acute inflammation in EAE.
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