ArticleJournal of neuroinflammation2018
Neuropeptide regulation of adaptive immunity in the tibia fracture model of complex regional pain syndrome.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
What it found
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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
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Pooled it
- Beliefs, attitudes, knowledge, and behaviours of physical therapists towards pediatric complex regional pain syndrome.World journal of clinical pediatrics · 2026Article
- The neuroimmune axis and chronic pain disorders.iScience · 2026Review
- A pilot imaging mass cytometry study of cutaneous nerve-immune cell interactions in post-herpetic neuralgia.Frontiers in immunology · 2026Article
- Clinical Outcomes of Pregabalin Therapy in Adults with Type I Complex Regional Pain Syndrome: A Case Series.Journal of pain research · 2026Article
- Article
- [Biomarkers in complex regional pain syndrome].Schmerz (Berlin, Germany) · 2025Review
- The Effect of Fremanezumab on Pain in Patients with Complex Regional Pain Syndrome: Study Protocol of a Randomized, Double-Blind, Proof-of-Concept, Placebo-Controlled Trial.Brain sciences · 2025Article
- A brief review of complex regional pain syndrome and current management.Annals of medicine · 2024Review
- Bone metabolism in complex regional pain syndrome.Pain reports · 2024Article
- Article
- Alpha-7 Nicotinic Acetylcholine Receptor Activation Inhibits Trauma Induced Pronociceptive Autoimmune Responses.The journal of pain · 2024Article
- Transient immune activation without loss of intraepidermal innervation and associated Schwann cells in patients with complex regional pain syndrome.Journal of neuroinflammation · 2024Article
- Microbiota-Accessible Boron-Containing Compounds in Complex Regional Pain Syndrome.Medicina (Kaunas, Lithuania) · 2023Review
- The Role of Neuroinflammation in Complex Regional Pain Syndrome: A Comprehensive Review.Journal of pain research · 2023Review
- Autonomic Regulation of Nociceptive and Immunologic Changes in a Mouse Model of Complex Regional Pain Syndrome.The journal of pain · 2022Article
- The autoimmune aetiology of unexplained chronic pain.Autoimmunity reviews · 2022Review
- Sex-Specific B Cell and Anti-Myelin Autoantibody Response After Peripheral Nerve Injury.Frontiers in cellular neuroscience · 2022Article
- Autoimmune regulation of chronic pain.Pain reports · 2021Review
- Animal Models of Complex Regional Pain Syndrome Type I.Journal of pain research · 2021Review
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 2 countries.
Funding
Abstract
backgroundBoth dysfunctional neuropeptide signaling and immune system activation are characteristic of complex regional pain syndrome (CRPS). Unknown is whether substance P (SP) or calcitonin gene-related peptide (CGRP) support autoantibody production and, consequently, nociceptive sensitization.
methodsThese experiments involved the use of a well-characterized tibia fracture model of CRPS. Mice deficient in SP expression (Tac1
resultsFunctional SP and CGRP signaling were required both for the full development of nociceptive sensitization after fracture and the deposition of IgM in skin and neural tissues. Furthermore, the passive transfer of serum from wildtype but not neuropeptide-deficient mice to fractured muMT mice caused enhanced allodynia and postural unweighting. Langerhans cells were increased in number in the skin of fracture mice and CRPS patients, and those increases in mice were reduced in neuropeptide signaling-deficient animals. Unexpectedly, Langerhans cell-deficient mice showed normal nociceptive sensitization after fracture. However, the increased expression of Krt16 after tibia fracture was not seen in neuropeptide-deficient mice.
conclusionsCollectively, these data support the hypothesis that neuropeptide signaling in the fracture limb of mice is required for autoantigenic IgM production and nociceptive sensitization. The mechanism may be related to neuropeptide-supported autoantigen expression.
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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.