AI Article Synopsis
- The study investigated how experimental autoimmune encephalomyelitis (EAE) affects remyelination in a pro-inflammatory environment by using two groups of female C57BL/6 mice.
- EAE mice showed accelerated remyelination with higher activation of immune cells and increased cytokine expression in the lesions compared to CFA control mice.
- Despite these immune responses, remyelination was actually reduced in EAE mice by day 14, indicating that a strong immune reaction may hinder myelin repair.
Article Abstract
Experimental autoimmune encephalomyelitis (EAE) and lysophosphatidylcholine (LPC)-induced demyelination were combined to study remyelination in a pro-inflammatory context. Two groups of female C57BL/6 mice were subjected either to EAE (EAE mice) or injected with just complete Freund's adjuvant (CFA) and pertussis toxin (PTX) followed by bilateral LPC and phosphate buffered saline injections in the corpus callosum on day 7 (CFA controls). Relative to CFA controls, EAE accelerated remyelination and increased innate immune cell activation, lymphocyte infiltration and cytokine gene expression in the LPC lesions. However, compared to CFA mice, remyelination was reduced (day 14) suggesting this aggressive immune response also compromised myelin repair in EAE mice.
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| http://dx.doi.org/10.1016/j.jneuroim.2019.576995 | DOI Listing |
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