ArticleNeurogastroenterology and motility2015
The GPR55 antagonist CID16020046 protects against intestinal inflammation.
Article in Neurogastroenterology and motility, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Endocannabinoid System as a Promising Therapeutic Target in Inflammatory Bowel Disease - A Systematic Review.Frontiers in immunology · 2021Pooled it
- Cannabigerol at the Interface of the Gut Microbiota and EndoCannabinoidome: Mechanistic Insights into Inflammation and Pain Modulation.Medical sciences (Basel, Switzerland) · 2026Review
- Targeting the LPI/GPR55 Axis in MAFLD and MASH: Novel Insights, Therapeutic Strategies and Future Directions.Liver international : official journal of the International Association for the Study of the Liver · 2026Review
- The dual roles of natural cannabidiol in combating oxidative stress and inflammation: A potential intestinal guardian.Redox biology · 2026Review
- The endocannabinoidome-gut microbiome-brain axis as a novel therapeutic target for autism spectrum disorder.Journal of biomedical science · 2025Review
- GPR55 Antagonist CID16020046 Suppresses Collagen-Induced Rheumatoid Arthritis by Suppressing Th1/Th17 Cells in Mice.International journal of molecular sciences · 2025Article
- Modulation of neuroinflammation and oxidative stress by targeting GPR55 - new approaches in the treatment of psychiatric disorders.Molecular psychiatry · 2024Review
- Secreted Phospholipases A2: Drivers of Inflammation and Cancer.International journal of molecular sciences · 2024Review
- GPR55 Antagonist CID16020046 Attenuates Obesity-Induced Airway Inflammation by Suppressing Chronic Low-Grade Inflammation in the Lungs.International journal of molecular sciences · 2024Article
- GPCRs involved in metabolic diseases: pharmacotherapeutic development updates.Acta pharmacologica Sinica · 2024Review
- Cannabinoids' Role in Modulating Central and Peripheral Immunity in Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Article
- Pharmacohistory of Cannabis Use-A New Possibility in Future Drug Development for Gastrointestinal Diseases.International journal of molecular sciences · 2023Review
- A comprehensive survival and prognosis analysis of GPR55 expression in hepatocellular carcinoma.Aging · 2023Article
- Lysophosphatidylglucoside/GPR55 signaling promotes foam cell formation in human M2c macrophages.Scientific reports · 2023Article
- Article
- Altered endocannabinoidome bioactive lipid levels accompany reduced DNBS-induced colonic inflammation in germ-free mice.Lipids in health and disease · 2023Article
- CID16020046, a GPR55 antagonist, attenuates sepsis‑induced acute kidney injury.Molecular medicine reports · 2022Article
- Critical roles of G protein-coupled receptors in regulating intestinal homeostasis and inflammatory bowel disease.Mucosal immunology · 2022Review
- The Endocannabinoids-Microbiota Partnership in Gut-Brain Axis Homeostasis: Implications for Autism Spectrum Disorders.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundG protein-coupled receptor 55 (GPR55) is a lysophospholipid receptor responsive to certain cannabinoids. The role of GPR55 in inflammatory processes of the gut is largely unknown. Using the recently characterized GPR55 inhibitor CID16020046, we determined the role of GPR55 in experimental intestinal inflammation and explored possible mechanisms of action.
methodsColitis was induced by either 2.5% dextran sulfate sodium (DSS) supplemented in the drinking water of C57BL/6 mice or by a single intrarectal application of trinitrobenzene sulfonic acid (TNBS). KEY
resultsDaily application of CID16020046 (20 mg/kg) significantly reduced inflammation scores and myeloperoxidase (MPO) activity. In the DSS colitis model, levels of tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β), and the expression of cyclooxygenase (Cox)-2 and signal transducer and activator of transcription 3 (STAT-3) were reduced in colon tissues while in TNBS-induced colitis, levels of Cox-2, IL-1β and IL-6 were significantly lowered. Evaluation of leukocyte recruitment by flow cytometry indicated reduced presence of lymphocytes and macrophages in the colon following GPR55 inhibition in DSS-induced colitis. In J774A.1 mouse macrophages, inhibition of GPR55 revealed reduced migration of macrophages and decreased CD11b expression, suggesting that direct effects of CID16020046 on macrophages may have contributed to the improvement of colitis. GPR55(-/-) knockout mice showed reduced inflammation scores as compared to wild type mice in the DSS model suggesting a pro-inflammatory role in intestinal inflammation. CONCLUSIONS & INFERENCES: Pharmacological blockade of GPR55 reduces experimental intestinal inflammation by reducing leukocyte migration and activation, in particular that of macrophages. Therefore, CID16020046 represents a possible drug for the treatment of bowel inflammation.
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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.