ArticleFrontiers in immunology2020
Sulfatide Inhibits HMGB1 Secretion by Hindering Toll-Like Receptor 4 Localization Within Lipid Rafts.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Lipid metabolism in moyamoya disease: Emerging evidence, vascular remodeling, and therapeutic implications.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Review
- Expression and clinical significance of S100A8/9 in adults with secondary phagocytic lymphohistiocytosis.Frontiers in molecular biosciences · 2025Article
- Diverse NKT cells regulate early inflammation and neurological outcomes after cardiac arrest and resuscitation.Science translational medicine · 2024Article
- Lipidomic Approaches in Common and Rare Cerebrovascular Diseases: The Discovery of Unconventional Lipids as Novel Biomarkers.International journal of molecular sciences · 2023Review
- Relationship of Sulfatides Physiological Function and Peroxisome Proliferator-Activated Receptor α.Neurochemical research · 2023Review
- Chronic brain damage in HIV-infected individuals under antiretroviral therapy is associated with viral reservoirs, sulfatide release, and compromised cell-to-cell communication.Cellular and molecular life sciences : CMLS · 2023Article
- Lipidomic analysis of brain and hippocampus from mice fed with high-fat diet and treated with fecal microbiota transplantation.Nutrition & metabolism · 2023Article
- Using Untargeted LC-MS Metabolomics to Identify the Association of Biomarkers in Cattle Feces with Marbling Standard Longissimus Lumborum.Animals : an open access journal from MDPI · 2022Article
- The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022Review
- The repertoire of protein-sulfatide interactions reveal distinct modes of sulfatide recognition.Frontiers in molecular biosciences · 2022Review
- The etiology and pathogenesis of type 1 diabetes - A personal, non-systematic review of possible causes, and interventions.Frontiers in endocrinology · 2022Review
- Plasma Lipid Profiling Contributes to Untangle the Complexity of Moyamoya Arteriopathy.International journal of molecular sciences · 2021Observational
- Article
- Multiplicity of Glycosphingolipid-Enriched Microdomain-Driven Immune Signaling.International journal of molecular sciences · 2021Review
- Sulfatides are endogenous ligands for the TLR4-MD-2 complex.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The high mobility group box 1 (HMGB1) is a well-known late mediator of sepsis, secreted by multiple stimuli, involving pathways, such as the mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) pathways, and reactive oxygen species (ROS) under inflammation. Sulfatide, in contrast, is a sphingolipid commonly found in myelin sheets with a disputed immunological role. We sought to determine the immunological characteristics of sulfatide in the periphery by analyzing the secretion of HMGB1 triggered by lipopolysaccharide (LPS) stimulation in Raw 264.7 cells. Suppression of HMGB1 secretion by inhibiting its cytosolic translocation was observed after pre-treatment with sulfatide before LPS stimulation. Further analysis of the downstream molecules of toll-like receptor (TLR) signaling revealed suppression of c-Jun N-terminal kinase (JNK) phosphorylation and p65 translocation. LPS-mediated ROS production was also decreased when sulfatide pre-treatment was provided, caused by the down-regulation of the phosphorylation of activators, such as IRAK4 and TBK1. Investigation of the upstream mechanism that encompasses all the aforementioned inhibitory characteristics unveiled the involvement of lipid rafts. In addition to the co-localization of biotinylated sulfatide and monosialotetrahexosylganglioside, a decrease in LPS-induced co-localization of TLR4 and lipid raft markers was observed when sulfatide treatment was given before LPS stimulation. Overall, sulfatide was found to exert its anti-inflammatory properties by hindering the co-localization of TLR4 and lipid rafts, nullifying the effect of LPS on TLR4 signaling. Similar effects of sulfatide were also confirmed in the LPS-mediated murine experimental sepsis model, showing decreased levels of serum HMGB1, increased survivability, and reduced pathological severity.
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