ArticleJournal of neurochemistry2016
Inhibition of myeloperoxidase at the peak of experimental autoimmune encephalomyelitis restores blood-brain barrier integrity and ameliorates disease severity.
Article in Journal of neurochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 73 citations in OpenAlex.
- Complementary PET and MRI of myeloperoxidase activity as a noninvasive surrogate for tissue acrolein in experimental neuroinflammation.NeuroImage · 2026Article
- Comprehensive Proteomic Profiling Reveals Dysregulation of Angiogenesis and Inflammatory Pathways in the Brains of SIRT3 Knockout Mice.Brain sciences · 2026Article
- Interaction Between Neutrophils and Elements of the Blood-Brain Barrier in the Context of Multiple Sclerosis and Ischemic Stroke.International journal of molecular sciences · 2025Review
- The emerging role of neutrophil extracellular traps in autoimmune and autoinflammatory diseases.MedComm · 2025Review
- Article
- The neutrophil extracellular traps in neurological diseases: an update.Clinical and experimental immunology · 2024Review
- Environment-sensitive turn-on fluorescent probe enables live cell imaging of myeloperoxidase activity during NETosis.Communications chemistry · 2024Article
- Temporal Dynamics of Oxidative Stress and Inflammation in Bronchopulmonary Dysplasia.International journal of molecular sciences · 2024Review
- Role of Myeloperoxidase, Oxidative Stress, and Inflammation in Bronchopulmonary Dysplasia.Antioxidants (Basel, Switzerland) · 2024Review
- The Role of Neutrophils in Multiple Sclerosis and Ischemic Stroke.Brain sciences · 2024Review
- Myeloperoxidase Gene Deletion Causes Drastic Microbiome Shifts in Mice and Does Not Mitigate Dextran Sodium Sulphate-Induced Colitis.International journal of molecular sciences · 2024Article
- Sterile inflammation induces vasculopathy and chronic lung injury in murine sickle cell disease.Free radical biology & medicine · 2024Article
- mRNA expression profile reveals differentially expressed genes in splenocytes of experimental autoimmune encephalomyelitis model.International journal of experimental pathology · 2023Article
- Auranofin Modulates Thioredoxin Reductase/Nrf2 Signaling in Peripheral Immune Cells and the CNS in a Mouse Model of Relapsing-Remitting EAE.Biomedicines · 2023Article
- Ferroptosis contributes to multiple sclerosis and its pharmacological targeting suppresses experimental disease progression.Cell death and differentiation · 2023Article
- Brain alarm by self-extracellular nucleic acids: from neuroinflammation to neurodegeneration.Journal of biomedical science · 2023Review
- Review
- Immune-Mediated Neuropathies: Pathophysiology and Management.International journal of molecular sciences · 2023Review
- Thiocyanate Reduces Motor Impairment in the hMPO-A53T PD Mouse Model While Reducing MPO-Oxidation of Alpha Synuclein in Enlarged LYVE1/AQP4 Positive Periventricular Glymphatic Vessels.Antioxidants (Basel, Switzerland) · 2022Article
- Myeloperoxidase as a Marker to Differentiate Mouse Monocyte/Macrophage Subsets.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Oxidative stress is thought to contribute to disease pathogenesis in the central nervous system (CNS) disease multiple sclerosis (MS). Myeloperoxidase (MPO), a potent peroxidase that generates toxic radicals and oxidants, is increased in the CNS during MS. However, the exact mechanism whereby MPO drives MS pathology is not known. We addressed this question by inhibiting MPO in mice with experimental autoimmune encephalomyelitis (EAE) using our non-toxic MPO inhibitor N-acetyl lysyltyrosylcysteine amide (KYC). We found that therapeutic administration of KYC for 5 days starting at the peak of disease significantly attenuated EAE disease severity, reduced myeloid cell numbers and permeability of the blood-brain barrier. These data indicate that inhibition of MPO by KYC restores blood-brain barrier integrity thereby limiting migration of myeloid cells into the CNS that drive EAE pathogenesis. In addition, these observations indicate that KYC may be an effective therapeutic agent for the treatment of MS. We propose that during experimental autoimmune encephalomyelitis (EAE) onset macrophages and neutrophils migrate into the CNS and upon activation release myeloperoxidase (MPO) that promotes disruption of the blood-brain barrier (BBB) and disease progression. KYC restores BBB function by inhibiting MPO activity and in so doing ameliorates disease progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.