ArticleRespiratory research2016
Administration of JTE013 abrogates experimental asthma by regulating proinflammatory cytokine production from bronchial epithelial cells.
Article in Respiratory research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Review
- Plasma lipids, amino acids, and their metabolic pathways as potential biomarkers for differential diagnosis of cold and heat syndrome asthma in children: a preliminary study.Frontiers in pediatrics · 2025Article
- PLK1 Mediates the Proliferation and Contraction of Airway Smooth Muscle Cells and Has a Role in T2-High Asthma with Neutrophilic Inflammation Model.Journal of inflammation research · 2025Article
- JTE-013 Alleviates Pulmonary Fibrosis by Affecting the RhoA/YAP Pathway and Mitochondrial Fusion/Fission.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Inhibition of Sphingosine-1-Phosphate Receptor 2 by JTE013 Enhanced Alveolar Bone Regeneration by Promoting Angiogenesis.International journal of molecular sciences · 2023Article
- Sphingosine-1-Phosphate Receptor 4 Attenuates Neutrophilic Airway Inflammation in Experimental Asthma via Repressing Proinflammatory Macrophage Activation.International journal of biological sciences · 2023Article
- Expression of sphingosine-1-phosphate receptor 2 is correlated with migration and invasion of human colon cancer cells: A preliminary clinical study.Oncology letters · 2022Article
- Endothelial S1pr2 regulates post-ischemic angiogenesis via AKT/eNOS signaling pathway.Theranostics · 2022Article
- Targeting S1PRs as a Therapeutic Strategy for Inflammatory Bone Loss Diseases-Beyond Regulating S1P Signaling.International journal of molecular sciences · 2021Review
- Human Keratinocytes Use Sphingosine 1-Phosphate and its Receptors to Communicate Staphylococcus aureus Invasion and Activate Host Defense.The Journal of investigative dermatology · 2019Article
- Blockage of sphingosine-1-phosphate receptor 2 attenuates allergic asthma in mice.British journal of pharmacology · 2019Article
- Article
- S1P Lyase Regulation of Thymic Egress and Oncogenic Inflammatory Signaling.Mediators of inflammation · 2017Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSphingosine-1-phosphate (S1P) is a bioactive phospholipid that acts as a signal transducer by binding to S1P receptors (S1PR) 1 to 5. The S1P/S1PRs pathway has been associated with remodeling and allergic inflammation in asthma, but the expression pattern of S1PR and its effects on non-immune cells have not been completely clarified. The aim of this study was to examine the contribution of the signaling of S1P and S1PRs expressed in airway epithelial cells (ECs) to asthma responses in mice.
methodsBronchial asthma was experimentally induced in BALB/c mice by ovalbumin (OVA) sensitization followed by an OVA inhalation challenge. The effects of S1PR antagonists on the development of asthma were analyzed 24 h after the OVA challenge.
resultsImmunohistological analysis revealed S1PR1-3 expression on mouse airway ECs. Quantitative real-time polymerase chain reaction demonstrated that S1P greatly stimulated the induction of CCL3 and TIMP2 mRNA in human airway ECs, i.e., BEAS-2B cells, in a dose-dependent manner. Pretreatment with the S1PR2 antagonist JTE013 inhibited the CCL3 gene expression in BEAS-2B cells. Immunohistological analysis also showed that the expression level of CCL3 was attenuated by JTE013 in asthmatic mice. Furthermore, JTE013 as well as anti-CCL3 antibody attenuated allergic responses. Intratracheal administration of JTE013 also attenuated eosinophilic reactions in bronchoalveolar lavage fluids. S1P induced transcription factor NFκB activation, while JTE013 greatly reduced the NFκB activation.
conclusionsJTE013 attenuated allergic airway reactions by regulating CCL3 production from bronchial ECs. The intratracheal administration of JTE013 may be a promising therapeutic strategy for bronchial asthma.
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