ArticlePain2019
Cathepsin E in neutrophils contributes to the generation of neuropathic pain in experimental autoimmune encephalomyelitis.
Article in Pain, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Fucoidan as a Promising Drug for Pain Treatment: Systematic Review and Meta-Analysis.Marine drugs · 2024Pooled it
- Construction and verification of a prognostic model of neutrophil-related genes in clear cell renal cell carcinoma.Translational andrology and urology · 2026Article
- Proteolytic profiling of human plasma reveals an immunoactive complement C3 fragment.The EMBO journal · 2025Article
- Neutrophils-astrocyte interactions in central nervous system inflammation.Cell death & disease · 2025Review
- Neutrophils, NETs and multiple sclerosis: a mini review.Frontiers in immunology · 2025Review
- The multifaceted roles of cathepsins in immune and inflammatory responses: implications for cancer therapy, autoimmune diseases, and infectious diseases.Biomarker research · 2024Review
- Cathepsins and neurological diseases: a Mendelian randomization study.Frontiers in neuroscience · 2024Article
- Article
- Neutrophil biology in injuries and diseases of the central and peripheral nervous systems.Progress in neurobiology · 2023Review
- The interaction between the nervous system and the stomatognathic system: from development to diseases.International journal of oral science · 2023Review
- One immune system plays many parts: The dynamic role of the immune system in chronic pain and opioid pharmacology.Neuropharmacology · 2023Review
- Neutrophils infiltrate sensory ganglia and mediate chronic widespread pain in fibromyalgia.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Pain-resolving immune mechanisms in neuropathic pain.Nature reviews. Neurology · 2023Review
- Characterization of pain-related behaviors and gene expression profiling of peripheral sensory ganglia in a mouse model of acute ankle sprain.Frontiers in behavioral neuroscience · 2023Article
- Mechanisms underlying the beneficial effects of physical exercise on multiple sclerosis: focus on immune cells.Frontiers in immunology · 2023Review
- Role of cathepsin K in the expression of mechanical hypersensitivity following intra-plantar inflammation.Scientific reports · 2022Article
- The Importance of CXCL1 in Physiology and Noncancerous Diseases of Bone, Bone Marrow, Muscle and the Nervous System.International journal of molecular sciences · 2022Review
- Microglial cathepsin E plays a role in neuroinflammation and amyloid β production in Alzheimer's disease.Aging cell · 2022Article
- Targeting Neuroimmune Interactions in Diabetic Neuropathy with Nanomedicine.Antioxidants & redox signaling · 2022Article
- Cathepsins in the Pathophysiology of Mucopolysaccharidoses: New Perspectives for Therapy.Cells · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pain is a frequent and disabling symptom in patients with multiple sclerosis (MS); however, the underlying mechanisms of MS-related pain are not fully understood. Here, we demonstrated that cathepsin E (CatE) in neutrophils contributes to the generation of mechanical allodynia in experimental autoimmune encephalomyelitis, an animal model of MS. We showed that CatE-deficient (CatE) mice were highly resistant to myelin oligodendrocyte glycoprotein (MOG35-55)-induced mechanical allodynia. After MOG35-55 immunization, neutrophils immediately accumulated in the dorsal root ganglion (DRG). Adoptive transfer of MOG35-55-stimulated wild-type neutrophils into the dorsal root ganglion induced mechanical allodynia in the recipient C57BL/6 mice. However, the pain threshold did not change when MOG35-55-stimulated CatE neutrophils were transferred into the recipient C57BL/6 mice. MOG35-55 stimulation caused CatE-dependent secretion of elastase in neutrophils. Behavioral analyses revealed that sivelestat, a selective neutrophil elastase inhibitor, suppressed mechanical allodynia induced by adoptively transferred MOG35-55-stimulated neutrophils. MOG35-55 directly bound to toll-like receptor 4, which led to increased production of CatE in neutrophils. Our findings suggest that inhibition of CatE-dependent elastase production in neutrophil might be a potential therapeutic target for pain in patients with MS.
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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.