ArticlePloS one2013
Liposomal lipopolysaccharide initiates TRIF-dependent signaling pathway independent of CD14.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 52 citations in OpenAlex.
- Acinetobacter baumannii lipooligosaccharide core region promotes CD14-dependent TLR4 endocytosis and enhances pathogenicity through interferon-β production.PLoS pathogens · 2026Article
- Zfand5 terminates TLR3/4 signaling and necroptosis by targeting TRIF to the proteasome for degradation.Cell death & disease · 2026Article
- Dietary Synbiotic Attenuated the Intestinal Inflammation in Weaned Piglets Challenged withAnimals : an open access journal from MDPI · 2025Article
- A detoxified TLR4 agonist inhibits tumour growth and lung metastasis of osteosarcoma by promoting CD8+ cytotoxic lymphocyte infiltration.BJC reports · 2025Article
- The Importance of Including Maternal Immune Activation in Animal Models of Hypoxic-Ischemic Encephalopathy.Biomedicines · 2024Article
- Metabolic Endotoxemia: From the Gut to Neurodegeneration.International journal of molecular sciences · 2024Review
- Intranasal administration of a synthetic TLR4 agonist INI-2004 significantly reduces allergy symptoms following therapeutic administration in a murine model of allergic sensitization.Frontiers in immunology · 2024Article
- Phage-resistance alters Lipid A reactogenicity: a new strategy for LPS-based conjugate vaccines againstFrontiers in immunology · 2024Article
- Role of CD14 in human disease.Immunology · 2023Review
- Bacterial extracellular vesicles repress the vascular protective factor RNase1 in human lung endothelial cells.Cell communication and signaling : CCS · 2023Article
- Bacterial vesicles block viral replication in macrophages via TLR4-TRIF-axis.Cell communication and signaling : CCS · 2023Article
- Terminal uridyltransferase 7 regulates TLR4-triggered inflammation by controlling Regnase-1 mRNA uridylation and degradation.Nature communications · 2021Article
- TLR4 and CD14 trafficking and its influence on LPS-induced pro-inflammatory signaling.Cellular and molecular life sciences : CMLS · 2021Review
- An alternative model for type I interferon induction downstream of human TLR2.The Journal of biological chemistry · 2020Article
- Therapeutic and Preventive Effects ofEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Alveolar-Capillary Membrane-Related Pulmonary Cells as a Target in Endotoxin-Induced Acute Lung Injury.International journal of molecular sciences · 2019Review
- Arid5a Regulation and the Roles of Arid5a in the Inflammatory Response and Disease.Frontiers in immunology · 2019Review
- Diverse pro-inflammatory endotoxin recognition systems of mammalian innate immunity.F1000Research · 2018Review
- Dingchuan tang essential oil inhibits the production of inflammatory mediators via suppressing the IRAK/NF-κB, IRAK/AP-1, and TBK1/IRF3 pathways in lipopolysaccharide-stimulated RAW264.7 cells.Drug design, development and therapy · 2018Article
- The ubiquitin ligase ZNRF1 promotes caveolin-1 ubiquitination and degradation to modulate inflammation.Nature communications · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipopolysaccharide (LPS) is recognized by CD14 with Toll-like receptor 4 (TLR4), and initiates 2 major pathways of TLR4 signaling, the MyD88-dependent and TRIF-dependent signaling pathways. The MyD88-dependent pathway induces inflammatory responses such as the production of TNF-α, IL-6, and IL-12 via the activation of NFκB and MAPK. The TRIF-dependent pathway induces the production of type-I IFN, and RANTES via the activation of IRF-3 and NFκB, and is also important for the induction of adaptive immune responses. CD14 plays a critical role in initiating the TRIF-dependent signaling pathway response to LPS, to support the internalization of LPS via endocytosis. Here, we clearly demonstrate that intracellular delivery of LPS by LPS-formulated liposomes (LPS-liposomes) initiate only TRIF-dependent signaling via clathrin-mediated endocytosis, independent of CD14. In fact, LPS-liposomes do not induce the production of TNF-α and IL-6 but induce RANTES production in peritoneal macrophages. Additionally, LPS-liposomes could induce adaptive immune responses effectively in CD14-deficient mice. Collectively, our results strongly suggest that LPS-liposomes are useful as a TRIF-dependent signaling-based immune adjuvant without inducing unnecessary inflammation.
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