ArticleScience translational medicine2011
CXCL5 mediates UVB irradiation-induced pain.
Article in Science translational medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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
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Who cites it
60 citing papers in PubMed, 113 citations in OpenAlex.
- Targeting CXCR2 in Nociceptive Sensory Neurons Offers Novel Therapeutic Potentials for Postoperative Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- CXCL7/CXCR2 in the paraventricular thalamus mediates obesity-related pain.Journal of neuroinflammation · 2026Article
- Conditioned medium from painful non-NF2 schwannomatosis tumors increases pain behaviors in mice.Scientific reports · 2025Article
- Investigating Snake-Venom-Induced Dermonecrosis and Inflammation Using an Ex Vivo Human Skin Model.Toxins · 2024Article
- CXCL5 activates CXCR2 in nociceptive sensory neurons to drive joint pain and inflammation in experimental gouty arthritis.Nature communications · 2024Article
- Transcriptome Analysis of the Mouse Medial Prefrontal Cortex in a Chronic Constriction Injury Model.Neuromolecular medicine · 2023Article
- Monoterpenoid aryl hydrocarbon receptor allosteric antagonists protect against ultraviolet skin damage in female mice.Nature communications · 2023Article
- 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
- Inflammation and Infection in Pain and the Role of GPR37.International journal of molecular sciences · 2022Review
- Photoprotective Effects of Cannabidiol against Ultraviolet-B-Induced DNA Damage and Autophagy in Human Keratinocyte Cells and Mouse Skin Tissue.Molecules (Basel, Switzerland) · 2022Article
- NRF2 in dermatological disorders: Pharmacological activation for protection against cutaneous photodamage and photodermatosis.Free radical biology & medicine · 2022Review
- Review
- Altered Plasma Proteins in Myogenous Temporomandibular Disorders.Journal of clinical medicine · 2022Article
- The beneficial role of companion animals in translational pain research.Frontiers in pain research (Lausanne, Switzerland) · 2022Review
- IMT504 Provides Analgesia by Modulating Cell Infiltrate and Inflammatory Milieu in a Chronic Pain Model.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Article
- Sensory defunctionalization induced by 8% topical capsaicin treatment in a model of ultraviolet-B-induced cutaneous hyperalgesia.Experimental brain research · 2021Article
- Hsa-miR-605 regulates the proinflammatory chemokine CXCL5 in complex regional pain syndrome.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Article
- Identification of key candidate genes in local dorsal root ganglion inflammation by integrated bioinformatics analysis.Experimental and therapeutic medicine · 2021Article
- Pain Phenotypes in Rare Musculoskeletal and Neuromuscular Diseases.Neuroscience and biobehavioral reviews · 2021Review
- Mast Cells and Skin and Breast Cancers: A Complicated and Microenvironment-Dependent Role.Cells · 2021Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Many persistent pain states (pain lasting for hours, days, or longer) are poorly treated because of the limitations of existing therapies. Analgesics such as nonsteroidal anti-inflammatory drugs and opioids often provide incomplete pain relief and prolonged use results in the development of severe side effects. Identification of the key mediators of various types of pain could improve such therapies. Here, we tested the hypothesis that hitherto unrecognized cytokines and chemokines might act as mediators in inflammatory pain. We used ultraviolet B (UVB) irradiation to induce persistent, abnormal sensitivity to pain in humans and rats. The expression of more than 90 different inflammatory mediators was measured in treated skin at the peak of UVB-induced hypersensitivity with custom-made polymerase chain reaction arrays. There was a significant positive correlation in the overall expression profiles between the two species. The expression of several genes [interleukin-1β (IL-1β), IL-6, and cyclooxygenase-2 (COX-2)], previously shown to contribute to pain hypersensitivity, was significantly increased after UVB exposure, and there was dysregulation of several chemokines (CCL2, CCL3, CCL4, CCL7, CCL11, CXCL1, CXCL2, CXCL4, CXCL7, and CXCL8). Among the genes measured, CXCL5 was induced to the greatest extent by UVB treatment in human skin; when injected into the skin of rats, CXCL5 recapitulated the mechanical hypersensitivity caused by UVB irradiation. This hypersensitivity was associated with the infiltration of neutrophils and macrophages into the dermis, and neutralizing the effects of CXCL5 attenuated the abnormal pain-like behavior. Our findings demonstrate that the chemokine CXCL5 is a peripheral mediator of UVB-induced inflammatory pain, likely in humans as well as rats.
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What OpenQuestion holds
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.