ArticleFundamental & clinical pharmacology2018
Inhibition of spinal p38 MAPK prevents articular neutrophil infiltration in experimental arthritis via sympathetic activation.
Article in Fundamental & clinical pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- [Research progress on the pathogenesis and clinical treatment of cirrhotic cardiomyopathy].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- Review of Perioperative Music Medicine: Mechanisms of Pain and Stress Reduction Around Surgery.Frontiers in medicine · 2022Review
- Electroacupuncture at ST36 (Journal of inflammation research · 2022Article
- Lipoxin A4-Mediated p38 MAPK Signaling Pathway Protects Mice Against Collagen-Induced Arthritis.Biochemical genetics · 2021Article
- Driving βFrontiers in immunology · 2021Article
- ASK1 inhibition: a therapeutic strategy with multi-system benefits.Journal of molecular medicine (Berlin, Germany) · 2020Review
- The role of neutrophils in neuro-immune modulation.Pharmacological research · 2020Review
- From neuroimunomodulation to bioelectronic treatment of rheumatoid arthritis.Bioelectronics in medicine · 2018Article
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Authors and funding
8 authors at 4 institutions in 4 countries.
Funding
Abstract
The central nervous system controls the innate immunity by modulating efferent neuronal networks. Recently, we have reported that central brain stimulation inhibits inflammatory responses. In the present study, we investigate whether spinal p38 mitogen-activated protein kinase (MAPK) affects joint inflammation in experimental arthritis. Firstly, we observed that intra-articular administration of zymosan in mice induces the phosphorylation of the spinal cord p38 MAPK. In addition, we demonstrated that spinal p38 MAPK inhibition with intrathecal injection of SB203580, a conventional and well-characterized inhibitor, prevents knee joint neutrophil recruitment, edema formation, experimental score and cytokine production. This local anti-inflammatory effect was completely abolished with chemical sympathectomy (guanethidine) and beta-adrenergic receptors blockade (nadolol). In conclusion, our results suggest that pharmacological strategies involving the modulation of spinal p38 MAPK circuit can prevent joint inflammation via sympathetic networks and beta-adrenoceptors activation.
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