ArticleJournal of neuroinflammation2025
Neuroinflammation causes mitral cell dysfunction and olfactory impairment in a multiple sclerosis model.
Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Glial pathology networks reveal early olfactory vulnerability in post mortem human Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Dynamics of neutrophilia at the neurovascular unit arising from repeated pulmonary inflammation.Journal of neuroinflammation · 2026Article
- Lipopolysaccharide-Induced Nasal Inflammation Swiftly Spreads Into the Olfactory Bulb, Accelerating its Network Activity and Uncoupling it from Breathing.Inflammation · 2026Article
- Comparative Effects of Anti-Inflammatory Therapies on Olfactory Bulb Histopathology and Olfactory Function in a Rat Model of Experimental Allergic Rhinitis.Journal of inflammation research · 2026Article
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Authors and funding
13 authors.
Funding
Abstract
backgroundOlfactory dysfunction is an underestimated symptom in multiple sclerosis (MS). Here, we examined the pathogenic mechanisms underlying inflammation-induced dysfunction of the olfactory bulb using the animal model of MS, experimental autoimmune encephalomyelitis (EAE).
resultsReduced olfactory function in EAE was associated with the degeneration of short-axon neurons, immature neurons, and both mitral and tufted cells, along with their synaptic interactions and axonal repertoire. To dissect the mechanisms underlying the susceptibility of mitral cells, the main projection neurons of the olfactory bulb, we profiled their responses to neuroinflammation by single-nucleus RNA sequencing followed by functional validation. Neuroinflammation resulted in the induction of potassium channel transcripts in mitral cells, which was reflected in increased halothane-induced outward currents of these cells, likely contributing to the impaired olfaction in EAE animals.
conclusionThis study reveals the crucial role of mitral cells and their potassium channel activity in the olfactory bulb during EAE, thereby enhancing our understanding of neuroinflammation-induced neurodegeneration in MS.
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