Loss of Axl receptor increases inflammation and delays myelin debris clearance in EAE
Author Information
Author(s): Jason G Weinger, Celia F Brosnan, Olivier Loudig, Michael F Goldberg, Fernando Macian, Heather A Arnett, Anne L Prieto, Vladislav Tsiperson, Bridget Shafit-Zagardo
Primary Institution: Albert Einstein College of Medicine
Hypothesis
Axl is important in minimizing immune-mediated CNS damage by dampening inflammation and aiding in debris clearance.
Conclusion
Axl deficiency leads to more severe EAE symptoms and greater spinal cord damage due to increased inflammation and impaired debris clearance.
Supporting Evidence
- Axl-/- mice showed significantly more severe EAE symptoms than WT mice.
- Spinal cord lesions in Axl-/- mice had larger inflammatory cuffs and more demyelination.
- Fewer activated microglia/macrophages were found in Axl-/- lesions compared to WT.
- Axl-/- mice had more Oil-Red-O staining, indicating inefficient clearance of myelin debris.
- More SMI32+ axons were observed in Axl-/- mice, indicating greater axonal damage.
Takeaway
Mice without the Axl receptor get sicker from a brain disease because they can't clean up the mess as well as mice with Axl.
Methodology
WT and Axl-/- mice were immunized with MOG peptide and monitored for clinical signs of EAE, with analysis of spinal cord pathology and immune responses.
Limitations
The study primarily focuses on acute EAE and may not fully represent chronic phases or other models of CNS inflammation.
Participant Demographics
Mice were age and sex-matched, specifically 8 weeks old.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
Want to read the original?
Access the complete publication on the publisher's website