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Updated: Dec 28, 2025
Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis
Published on: September 9, 2022
ADAMTS13 ameliorates inflammatory responses in experimental autoimmune encephalomyelitis
Kaili Lu1, Lan Liu1, Xiaofeng Xu1
1Department of Neurology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, No. 600, Yishan Road, Xuhui District, Shanghai, China.
Background:
ADAMTS13 (a disintegrin and metalloprotease with a thrombospondin type 1 motif, member 13) plays a vital role in preventing microvascular thrombosis and inflammation. Reduced ADAMTS13 levels in plasma have been detected in multiple sclerosis (MS) patients. In the present study, we have determined the role of ADAMTS13 in the disease progression of MS using a mouse model of experimental autoimmune encephalomyelitis (EAE).
Methods:
Female C57BL/6 mice were immunized with MOG35-55 peptide and then treated with ADAMTS13 or vehicle in preventive and therapeutic settings. Mice were analyzed for clinical deficit, white matter demyelination and inflammatory cell infiltration. To explore the underlying mechanism, VWF expression and blood-spinal cord barriers (BSCB) were determined.
Results:
Plasma ADAMTS13 activity was suppressed in EAE mice. ADAMTS13-treated EAE mice exhibited an ameliorated disease course, reduced demyelination, and decreased T lymphocyte, neutrophil and monocyte infiltration into the spinal cord. Consistently, ADAMTS13 treatment reduced VWF levels and inhibited BSCB breakdown in the spinal cords of EAE mice. However, leukocytes in the blood and spleen of EAE mice remained unaffected by ADAMTS13 administration.
Conclusion:
Our results demonstrate that ADAMTS13 treatment ameliorates inflammatory responses, demyelination and disease course in EAE mice. Therefore, our study suggests that ADAMTS13 may represent a potential therapeutic strategy for MS patients.
Insights
ADAMTS13 (a disintegrin and metalloprotease with a thrombospondin type 1 motif, member 13) treatment ameliorates multiple sclerosis (MS) progression in a mouse model. This suggests ADAMTS13 may be a promising therapeutic strategy for MS patients.
Area of Science:
- Neuroimmunology
- Hematology
Background:
- ADAMTS13 (a disintegrin and metalloprotease with a thrombospondin type 1 motif, member 13) is crucial for preventing microvascular thrombosis and inflammation.
- Reduced ADAMTS13 levels are observed in multiple sclerosis (MS) patients.
- The role of ADAMTS13 in MS disease progression was investigated using a mouse model.
Purpose of the Study:
- To determine the therapeutic potential of ADAMTS13 in experimental autoimmune encephalomyelitis (EAE), a mouse model of MS.
- To evaluate the impact of ADAMTS13 on disease course, demyelination, and inflammatory infiltration in the EAE model.
Main Methods:
- Female C57BL/6 mice were induced with EAE using MOG35-55 peptide.
- Mice received ADAMTS13 or vehicle treatment in preventive and therapeutic settings.
- Clinical deficits, demyelination, inflammatory cell infiltration, VWF expression, and blood-spinal cord barrier (BSCB) integrity were assessed.
Main Results:
- ADAMTS13 activity was suppressed in EAE mice.
- ADAMTS13 treatment ameliorated EAE, reducing demyelination and inflammatory cell infiltration in the spinal cord.
- ADAMTS13 administration reduced VWF levels and inhibited BSCB breakdown, but did not affect peripheral leukocytes.
Conclusions:
- ADAMTS13 treatment effectively ameliorates inflammatory responses, demyelination, and disease progression in the EAE mouse model.
- These findings suggest that ADAMTS13 holds potential as a therapeutic strategy for multiple sclerosis.
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