ArticleBrain pathology (Zurich, Switzerland)2020
IL-1β/IL-1R1 signaling induced by intranasal lipopolysaccharide infusion regulates alpha-Synuclein pathology in the olfactory bulb, substantia nigra and striatum.
Article in Brain pathology (Zurich, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Olfactory dysfunction in aging and neurodegenerative diseases.Ageing research reviews · 2021Pooled it
- Allergic disease as a risk factor for Parkinson's disease: a possible role of eosinophil.NPJ Parkinson's disease · 2026Article
- Orchestrating neuroinflammation: A symphony of Interleukin-1 and cell type-specific Interleukin-1 receptor type 1 signaling in the brain.Brain behavior and immunity integrative · 2026Article
- Dynamics of neutrophilia at the neurovascular unit arising from repeated pulmonary inflammation.Journal of neuroinflammation · 2026Article
- Aggregation and Propagation of α-Synuclein in Parkinson's Disease: A Bibliometric Perspective.Brain and behavior · 2025Article
- Dynamics of Neutrophilia at the Neurovascular Unit Arising from Repeated Pulmonary Inflammation.bioRxiv : the preprint server for biology · 2025Article
- IC100 blocks inflammasome activation induced by α-synuclein aggregates and ASC specks.NPJ Parkinson's disease · 2025Article
- Interleukin-1β depresses neuronal activity in the rat olfactory bulb even during odor stimulation.PloS one · 2025Article
- Exploring the diagnostic potential of IL1R1 in depression and its association with lipid metabolism.Frontiers in pharmacology · 2025Article
- The application of fecal microbiota transplantation in Parkinson's disease.Frontiers in aging neuroscience · 2025Review
- Does COVID-19 Trigger the Risk for the Development of Parkinson's Disease? Therapeutic Potential of Vitamin C.Molecular neurobiology · 2024Review
- The Synergistic Effect Study of Lipopolysaccharide (LPS) and A53T-α-Synuclein: Intranasal LPS Exposure on the A53T-α-Synuclein Transgenic Mouse Model of Parkinson's Disease.Molecular neurobiology · 2024Article
- Review
- Locus coeruleus injury modulates ventral midbrain neuroinflammation during DSS-induced colitis.Research square · 2024Article
- Olfactory dysfunction and its related molecular mechanisms in Parkinson's disease.Neural regeneration research · 2024Review
- Microglial inhibition alleviates alpha-synuclein propagation and neurodegeneration in Parkinson's disease mouse model.NPJ Parkinson's disease · 2024Article
- Cytokine activity in Parkinson's disease.Neuronal signaling · 2023Review
- The Olfactory System: Basic Anatomy and Physiology for General Otorhinolaryngologists.Clinical and experimental otorhinolaryngology · 2023Review
- The Involvement of Neuroinflammation in the Onset and Progression of Parkinson's Disease.International journal of molecular sciences · 2023Review
- Chronic inflammation and the hallmarks of aging.Molecular metabolism · 2023Review
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Olfactory dysfunction is one of the early symptoms seen in Parkinson's disease (PD). However, the mechanisms underlying olfactory pathology that impacts PD disease progression and post-mortem appearance of alpha-Synuclein (α-Syn) inclusions in and beyond olfactory bulb in PD remain unclear. It has been suggested that environmental toxins inhaled through the nose can induce inflammation in the olfactory bulb (OB), where Lewy body (LB) is the first to be found, and then, spread to related brain regions. We hypothesize that OB inflammation triggers local α-Syn pathology and promotes its spreading to cause PD. In this study, we evaluated this hypothesis by intranasal infusion of lipopolysaccharides (LPS) to induce OB inflammation in mice and examined cytokines expression and PD-like pathology. We found intranasal LPS-induced microglia activation, inflammatory cytokine expression and α-Syn overexpression and aggregation in the OB via interleukin-1β (IL-1β)/IL-1 receptor type I (IL-1R1) dependent signaling. In addition, an aberrant form of α-Syn, the phosphorylated serine 129 α-Syn (pS129 α-Syn), was found in the OB, substantia nigra (SN) and striatum 6 weeks after the LPS treatment. Moreover, 6 weeks after the LPS treatment, mice showed reduced SN tyrosine hydroxylase, decreased striatal dopaminergic metabolites and PD-like behaviors. These changes were blunted in IL-1R1 deficient mice. Further studies found the LPS treatment inhibited IL-1R1-dependent autophagy in the OB. These results suggest that IL-1β/IL-1R1 signaling in OB play a vital role in the induction and propagation of aberrant α-Syn, which may ultimately trigger PD pathology.
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