ArticleBritish journal of pharmacology2008
Role of complement C5a in mechanical inflammatory hypernociception: potential use of C5a receptor antagonists to control inflammatory pain.
Article in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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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
33 citing papers in PubMed, 78 citations in OpenAlex.
- Trial
- Biphasic modulation of large-fiber excitability accompanied by dynamic nerve-intrinsic immune activation following CFA-induced peripheral inflammation in mice.Scientific reports · 2026Article
- Complement C3a and C5a Receptors Are Presented in Mouse Sciatic and Human Sural Nerves and Selectively Modulate the Neuronal Function of Large-Caliber Fibers in Mice.Journal of neurochemistry · 2025Article
- Inflammatory pain resolution by mouse serum-derived small extracellular vesicles.Brain, behavior, and immunity · 2025Article
- Autoantibodies cause nociceptive sensitization in a mouse model of degenerative osteoarthritis.Pain · 2024Article
- Schwann cell C5aR1 co-opts inflammasome NLRP1 to sustain pain in a mouse model of endometriosis.Nature communications · 2024Article
- The influence of sex on neuroimmune communication, pain, and physiology.Biology of sex differences · 2024Review
- Inflammatory pain resolution by mouse serum-derived small extracellular vesicles.bioRxiv : the preprint server for biology · 2024Article
- Neutrophil biology in injuries and diseases of the central and peripheral nervous systems.Progress in neurobiology · 2023Review
- Emerging Approaches for the Management of Chemotherapy-Induced Peripheral Neuropathy (CIPN): Therapeutic Potential of the C5a/C5aR Axis.Pain and therapy · 2022Review
- The Interplay between Chronic Pain, Opioids, and the Immune System.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022Review
- Emerging Role of C5 Complement Pathway in Peripheral Neuropathies: Current Treatments and Future Perspectives.Biomedicines · 2021Review
- Immune Actions on the Peripheral Nervous System in Pain.International journal of molecular sciences · 2021Review
- Article
- The Complement System Component C5a Produces Thermal Hyperalgesia via Macrophage-to-Nociceptor Signaling That Requires NGF and TRPV1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- The Complement System in Neuropathic and Postoperative Pain.The open pain journal · 2016Article
- Bosentan, a mixed endothelin receptor antagonist, inhibits superoxide anion-induced pain and inflammation in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- Effect of gedunin on acute articular inflammation and hypernociception in mice.Molecules (Basel, Switzerland) · 2015Article
- Targeting the minor pocket of C5aR for the rational design of an oral allosteric inhibitor for inflammatory and neuropathic pain relief.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- The role of PAF/PAFR signaling in zymosan-induced articular inflammatory hyperalgesia.Naunyn-Schmiedeberg's archives of pharmacology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeC5a, a complement activation product, exhibits a broad spectrum of inflammatory activities particularly neutrophil chemoattraction. Herein, the role of C5a in the genesis of inflammatory hypernociception was investigated in rats and mice using the specific C5a receptor antagonist PMX53 (AcF-[OP(D-Cha)WR]). EXPERIMENTAL APPROACH: Mechanical hypernociception was evaluated with a modification of the Randall-Selitto test in rats and electronic pressure meter paw test in mice. Cytokines were measured by ELISA and neutrophil migration was determined by myeloperoxidase activity. KEY
resultsLocal pretreatment of rats with PMX53 (60-180 microg per paw) inhibited zymosan-, carrageenan-, lipopolysaccharide (LPS)- and antigen-induced hypernociception. These effects were associated with C5a receptor blockade since PMX53 also inhibited the hypernociception induced by zymosan-activated serum and C5a but not by the direct-acting hypernociceptive mediators, prostaglandin E(2) and dopamine. Underlying the C5a hypernociceptive mechanisms, PMX53 did not alter the cytokine release induced by inflammatory stimuli. However, PMX53 inhibited cytokine-induced hypernociception. PMX53 also inhibited the recruitment of neutrophils induced by zymosan but not by carrageenan or LPS, indicating an involvement of neutrophils in the hypernociceptive effect of C5a. Furthermore, the C5a-induced hypernociception was reduced in neutrophil-depleted rats. Extending these findings in rats, blocking C5a receptors also reduced zymosan-induced joint hypernociception in mice. CONCLUSIONS AND IMPLICATIONS: These results suggest that C5a is an important inflammatory hypernociceptive mediator, acting by a mechanism independent of hypernociceptive cytokine release, but dependent on the presence of neutrophils. Therefore, we suggest that inhibiting the action of C5a has therapeutic potential in the control of inflammatory pain.
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