Maresin-1 attenuates neuroinflammation in EAE via metabolic reprogramming of disease-associated cell types

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Presentation Time: 02:15 PM - 03:30 PM
Poster Board Number: B898
Abstract ID: 6187

Presenting Author:
Insha Zahoor , Postdoctoral Fellow at Henry Ford Hlth.

Abstract:

Inflammation resolution is dysregulated in people affected with multiple sclerosis (MS) due to impaired metabolism of docosahexaenoic acid (DHA). We hypothesize that supplementing its downstream metabolite maresin 1 (MaR1) will alleviate inflammation and demyelination in a preclinical mouse model of MS; experimental allergic encephalomyelitis (EAE). Administration of the resolution agonist MaR1 mediated resolution and improved neurological outcome in the relapsing-remitting (RR) model of EAE. MaR1 induced metabolic changes in CD4, macrophages, microglia, and oligodendrocytes. It modulated the phenotype of disease-associated cell types by regulating their effector functions. It restored the impaired efferocytosis in EAE, promoting clearance of damaged myelin and dead cells; thereby lowering the disability with disease course. MaR1 is a potential interventional candidate to attenuate dysregulated inflammation to restore neurological deficits in EAE and other autoimmune diseases.