ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2013
Suppression of Toll-like receptor 4 activation by endogenous oxidized phosphatidylcholine, KOdiA-PC by inhibiting LPS binding to MD2.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Immunohistochemical Localization of MD2, a Co-Receptor of TLR4, in the Adult Mouse Brain.ACS chemical neuroscience · 2023Article
- Fat of the Gut: Epithelial Phospholipids in Inflammatory Bowel Diseases.International journal of molecular sciences · 2021Review
- Oxidized Phospholipids in Tumor Microenvironment Stimulate Tumor Metastasis via Regulation of Autophagy.Cells · 2021Article
- Review
- The effect of oxidized phospholipids on phenotypic polarization and function of macrophages.Free radical biology & medicine · 2017Review
- Targeting myeloid differentiation protein 2 by the new chalcone L2H21 protects LPS-induced acute lung injury.Journal of cellular and molecular medicine · 2017Article
- Role for phospholipid acyl chains and cholesterol in pulmonary infections and inflammation.Journal of leukocyte biology · 2016Review
- Discovery of new MD2 inhibitor from chalcone derivatives with anti-inflammatory effects in LPS-induced acute lung injury.Scientific reports · 2016Article
- Kdo2 -lipid A: structural diversity and impact on immunopharmacology.Biological reviews of the Cambridge Philosophical Society · 2015Review
- Accumulating evidence for a role of oxidized phospholipids in infectious diseases.Cellular and molecular life sciences : CMLS · 2015Review
- Lipid peroxidation generates biologically active phospholipids including oxidatively N-modified phospholipids.Chemistry and physics of lipids · 2014Review
- IRAK1/4-targeted anti-inflammatory action of caffeic acid.Mediators of inflammation · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveActivation of Toll-like receptor 4 (TLR4) triggers immune and inflammatory events by sensing endogenous danger signals as well as invading pathogens and contributes to the development of chronic inflammatory diseases. In this study, we investigated effect of 1-palmitoyl-2-(5-keto-6-octenedioyl)-sn-glycero-3-phosphocholine (KOdiA-PC), an oxidized phosphatidylcholine, on TLR4 activation and the underlying regulatory mechanism.
methodsRAW264.7 macrophages were used for the study. The levels of TNF-α, IFN-β, and COX-2 mRNA and protein were determined by quantitative PCR and ELISA, respectively. Activation of TLR4-signaling was examined by immunoblot and luciferase reporter assays. In vitro binding assay was performed to determine LPS binding to MD2. Macrophage migration was analyzed using a transwell-culture system.
resultsKOdiA-PC prevented the activation of TLR4-signaling components including ERK, JNK, p38, NF-κB, and IRF3 leading to decrease of TNF-α, IFN-β, and COX-2 expression. In vitro binding assay revealed that KOdiA-PC interrupted LPS binding to MD2, a TLR4 co-receptor. Consistently, KOdiA-PC suppressed LPS-induced macrophage migration.
conclusionThe results demonstrate that KOdiA-PC can modulate TLR4 activation by regulating ligand-receptor interaction. Therefore, endogenously generated, oxidized phospholipids may play a role in resolving inflammation by terminating TLR activation and macrophage recruitment to the inflamed site.
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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.