ArticleNature communications2024
CXCL5 activates CXCR2 in nociceptive sensory neurons to drive joint pain and inflammation in experimental gouty arthritis.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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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
51 citing papers in PubMed, 53 citations in OpenAlex.
- Associations of Serum CIRP and CXCL5 With Prognosis and Neutrophil Extracellular Traps in Pediatric Mycoplasma pneumoniae Pneumonia.The clinical respiratory journal · 2026Article
- TRPA1 Regulates Fibrosis-Associated Transcriptional Pathways in Human Lung Epithelial Cells.Basic & clinical pharmacology & toxicology · 2026Article
- Activating Transcription Factor 3 in Pain: A Molecular Regulator and Emerging Biomarker.Genes · 2026Review
- Targeting CXCR2 in Nociceptive Sensory Neurons Offers Novel Therapeutic Potentials for Postoperative Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The alkaloid-rich extract of Piper sintenense Hatusima alleviates gouty inflammatory response via Nrf2-mediated antioxidant induction.Inflammopharmacology · 2026Article
- Multimetal-Doped Nanoenzymes Reprogram Macrophages for Immunotherapy of Gouty Arthritis.Advanced healthcare materials · 2026Article
- Proteomic analysis reveals divergent inflammatory mechanisms of COVID-associated Guillain-Barré syndrome.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Diabetic Wound Healing Enabled by a Tri-Functional MAX Phase via Cu Doping.Advanced healthcare materials · 2026Article
- Engineering technology of implantable galvanic cells for silencing the bone-neural axis in gouty arthritis therapy.Nature communications · 2026Article
- The microbiome across the prostate disease continuum: from health and BPH to prostatitis/CPPS and cancer.Oncogene · 2026Review
- TRPA1 and TRPM8 in Allergic Rhinitis and Chronic Rhinosinusitis: Emerging Role in Neuroimmune Inflammation.Biomedicines · 2026Review
- Correlation analysis of PGC-1β, HIF-1α and RETN with the degree of joint destruction in gouty arthritis.Journal of medical biochemistry · 2026Article
- Dendrophenol modulates the LRRK1/PIK3AP1 signaling axis: a novel strategy to mitigate inflammation and pyroptosis in gouty arthritis.BMC immunology · 2026Article
- Pentagalloyl glucose Suppresses MSU Crystal-Induced Gout Inflammation and Arachidonic Acid Production In Vitro and In Vivo.Research square · 2026Article
- Acetylshikonin alleviates gouty arthritis by increasing sirtuin1 expression and promoting lymphatic drainage.BMC pharmacology & toxicology · 2026Article
- Mast cell-expressed Mrgprb2/MRGPRX2 mediates gout pain and inflammation via a neuroimmune axis.JCI insight · 2026Article
- Neutrophil-initiated nociceptive ingrowth orchestrates inflammation resolution to potentiate bone regeneration.Bone research · 2026Article
- CXCL7/CXCR2 in the paraventricular thalamus mediates obesity-related pain.Journal of neuroinflammation · 2026Article
- Electroacupuncture ameliorates incisional pain via suppressing IL-33 signaling-related macrophage infiltration and ROS overproduction in incised skin.Chinese medicine · 2026Article
- Peripheral CD4Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 1 country.
Funding
Abstract
Gouty arthritis evokes joint pain and inflammation. Mechanisms driving gout pain and inflammation remain incompletely understood. Here we show that CXCL5 activates CXCR2 expressed on nociceptive sensory neurons to drive gout pain and inflammation. CXCL5 expression was increased in ankle joints of gout arthritis model mice, whereas CXCR2 showed expression in joint-innervating sensory neurons. CXCL5 activates CXCR2 expressed on nociceptive sensory neurons to trigger TRPA1 activation, resulting in hyperexcitability and pain. Neuronal CXCR2 coordinates with neutrophilic CXCR2 to contribute to CXCL5-induced neutrophil chemotaxis via triggering CGRP- and substance P-mediated vasodilation and plasma extravasation. Neuronal Cxcr2 deletion ameliorates joint pain, neutrophil infiltration and gait impairment in model mice. We confirmed CXCR2 expression in human dorsal root ganglion neurons and CXCL5 level upregulation in serum from male patients with gouty arthritis. Our study demonstrates CXCL5-neuronal CXCR2-TRPA1 axis contributes to gouty arthritis pain, neutrophil influx and inflammation that expands our knowledge of immunomodulation capability of nociceptive sensory neurons.
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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.