ArticleBritish journal of pharmacology1999
Cytokine-mediated inflammatory hyperalgesia limited by interleukin-4.
Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 219 citations in OpenAlex.
- Interleukin-4 induces CD11ceLife · 2025Article
- Interleukin-4 Induces the Release of Opioid Peptides from M1 Macrophages in Pathological Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- IL-4 induces M2 macrophages to produce sustained analgesia via opioids.JCI insight · 2020Article
- Advanced Technology for Gene Delivery with Homing Peptides to Spinal Cord through Systemic Circulation in Mice.Molecular therapy. Methods & clinical development · 2019Article
- Targeting Cytokines for Morphine Tolerance: A Narrative Review.Current neuropharmacology · 2019Review
- Article
- Divergent roles of immune cells and their mediators in pain.Rheumatology (Oxford, England) · 2018Review
- Chronic Pain in Inflammatory Arthritis: Mechanisms, Metrology, and Emerging Targets-A Focus on the JAK-STAT Pathway.Pain research & management · 2018Review
- Leishmania infection: painful or painless?Parasitology research · 2017Review
- Differential Impact of miR-21 on Pain and Associated Affective and Cognitive Behavior after Spared Nerve Injury in B7-H1 ko Mouse.Frontiers in molecular neuroscience · 2017Article
- An Animal Model of Modic Changes by Embedding Autogenous Nucleus Pulposus inside Subchondral Bone of Lumbar Vertebrae.Scientific reports · 2016Article
- IL4-10 Fusion Protein Is a Novel Drug to Treat Persistent Inflammatory Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- An early granulocyte colony-stimulating factor treatment attenuates neuropathic pain through activation of mu opioid receptors on the injured nerve.Scientific reports · 2016Article
- Age differences in cytokine expression under conditions of health using experimental pain models.Experimental gerontology · 2015Article
- Anti-inflammatory T-cell shift in neuropathic pain.Journal of neuroinflammation · 2015Article
- Methods for gene transfer to the central nervous system.Advances in genetics · 2014Review
- Herpes simplex virus-based nerve targeting gene therapy in pain management.Journal of pain research · 2014Review
- IL-4, JAK-STAT signaling, and pain.JAK-STAT · 2013Review
- Interleukin-1β increased the expression of protease-activated receptor 4 mRNA and protein in dorsal root ganglion neurons.Neurochemical research · 2013Article
- IL-4 and IL-13 inhibit IL-1β and TNF-α induced kinin B1 and B2 receptors through a STAT6-dependent mechanism.British journal of pharmacology · 2013Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The effect of IL-4 on responses to intraplantar (i.pl.) carrageenin, bradykinin, TNFalpha, IL-1beta, IL-8 and PGE2 was investigated in a model of mechanical hyperalgesia in rats. Also, the cellular source of the IL-4 was investigated. 2. IL-4, 30 min before the stimulus, inhibited responses to carrageenin, bradykinin, and TNFalpha, but not responses to IL-1beta, IL-8 and PGE2. 3. IL-4, 2 h before the injection of IL-1beta, did not affect the response to IL-1beta, whereas IL-4, 12 or 12+2 h before the IL-1beta, inhibited the hyperalgesia (-30%, -74%, respectively). 4. In murine peritoneal macrophages, murine IL-4 for 2 h before stimulation with LPS, inhibited (-40%) the production of IL-1beta but not PGE2. Murine IL-4 (for 16 h before stimulation with LPS) inhibited LPS-stimulated PGE2 but not IL-1beta. 5. Anti-murine IL-4 antibodies potentiated responses to carrageenin, bradykinin and TNFalpha, but not IL-1beta and IL-8, as well as responses to bradykinin in athymic rats but not in rats depleted of mast cells with compound 40/80. 6. These data suggest that IL-4 released by mast cells limits inflammatory hyperalgesia. During the early phase of the inflammatory response the mode of action of the IL-4 appears to be inhibition of the production TNFalpha, IL-1beta and IL-8. In the later phase of the response, in addition to inhibiting the production of pro-inflammatory cytokines, IL-4 also may inhibit the release of PGs.
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