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Cladribine modifies functional properties of microglia.
L Ø Jørgensen1,2,3, K H Hyrlov1,2,3, M L Elkjaer1,2,3
1Department of Neurology, Odense University Hospital, Odense, Denmark.
Clinical and Experimental Immunology
|June 4, 2020
Summary
Cladribine (CdA) affects activated microglia by reducing their function and migration at concentrations found in human cerebrospinal fluid. This suggests a direct impact on central nervous system cells beyond lymphocyte depletion.
Area of Science:
- Neuroimmunology
- Pharmacology
Background:
- Cladribine (CdA) is an oral prodrug for relapsing multiple sclerosis, known for lymphocyte depletion.
- CdA crosses the blood-brain barrier, indicating potential effects on central nervous system (CNS) resident cells.
Purpose of the Study:
- To investigate the impact of CdA on the phenotype and function of primary mouse microglia.
- To determine if CdA affects microglia at concentrations relevant to human cerebrospinal fluid (CSF).
Main Methods:
- Primary mouse microglia were stimulated with lipopolysaccharide (LPS) or interleukin-4 (IL-4) and treated with varying CdA concentrations.
- Assessed microglia viability, phagocytosis, morphology, random migration, gene expression (qPCR), and protein secretion (Meso Scale Discovery).
Main Results:
- Activated microglia, but not naive ones, were affected by CdA (0.1-1 μM) without viability loss.
- CdA (0.1-1 μM) reduced activated microglia's granularity, phagocytosis, and migration.
- Higher CdA concentration (10 μM) altered gene expression of inflammatory and anti-inflammatory markers in activated microglia.
Conclusions:
- Low CdA concentrations (0.1-1 μM) may induce a less activated microglia phenotype in the CNS.
- Upregulation of deoxycytidine kinase (DCK) in activated microglia may mediate CdA's effects.
- CdA might exert direct effects on CNS-resident microglia, offering a potential alternative therapeutic mechanism.
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