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Testing effects of glatiramer acetate and fingolimod in an infectious model of CNS immune surveillance
Cyd Castro-Rojas1, Krystin Deason1, Rehana Z Hussain1
1Department of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center at Dallas, TX, USA.
Abstract:
Immune surveillance of the CNS is critical for preventing infections; however, there is no accepted experimental model to assess the risk of infection when utilizing disease-modifying agents. We tested two approved agents for patients with multiple sclerosis (MS), glatiramer acetate and fingolimod, in an experimental model of CNS immune surveillance. C57BL/6 mice were infected with the ME49 strain of the neuroinvasive parasite Toxoplasma gondii (T. gondii) and then treated with GA and fingolimod. Neither treatment affected host survival; however, differences were observed in parasite load and in leukocyte numbers in the brains of infected animals. Here we demonstrate that this model could be a useful tool for analyzing immune surveillance.
Insights
This study introduces a new mouse model to assess central nervous system (CNS) immune surveillance risks with multiple sclerosis (MS) treatments. The model helps analyze how glatiramer acetate and fingolimod affect parasite load and brain leukocytes.
Area of Science:
- Neuroimmunology
- Infectious Disease Research
- Pharmacology
Background:
- Central nervous system (CNS) immune surveillance is vital for preventing infections.
- Existing experimental models are insufficient for evaluating infection risks associated with disease-modifying agents in multiple sclerosis (MS).
Purpose of the Study:
- To develop and validate an experimental model for assessing CNS immune surveillance.
- To evaluate the impact of glatiramer acetate (GA) and fingolimod on CNS immune responses during infection.
Main Methods:
- Utilized a C57BL/6 mouse model infected with Toxoplasma gondii (T. gondii).
- Administered glatiramer acetate (GA) and fingolimod to infected mice.
- Assessed host survival, parasite load, and leukocyte counts in the brain.
Main Results:
- Neither GA nor fingolimod significantly affected host survival.
- Differences in parasite load and brain leukocyte numbers were observed between treatment groups.
- The experimental model demonstrated utility in analyzing immune surveillance.
Conclusions:
- The developed T. gondii infection model in mice provides a viable platform for studying CNS immune surveillance.
- This model can aid in assessing potential infection risks associated with MS therapies like glatiramer acetate and fingolimod.
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