ArticleThe Journal of biological chemistry2015
Alteration of lysosome fusion and low-grade inflammation mediated by super-low-dose endotoxin.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Underlying Mechanism of Lysosomal Membrane Permeabilization in CNS Injury: A Literature Review.Molecular neurobiology · 2025Review
- Adaptor molecules mediate negative regulation of macrophage inflammatory pathways: a closer look.Frontiers in immunology · 2024Review
- Toll-interacting protein may affect doxorubicin resistance in hepatocellular carcinoma cell lines.Molecular biology reports · 2023Article
- Skin Cell and Tissue Responses to Cross-Linked Hyaluronic Acid in Low-Grade Inflammatory Conditions.International journal of inflammation · 2023Article
- TOLLIP Protein Expression Predicts Unfavorable Outcome in Renal Cell Carcinoma.International journal of molecular sciences · 2022Article
- Intravenous route to choroidal neovascularization by macrophage-disguised nanocarriers for mTOR modulation.Acta pharmaceutica Sinica. B · 2022Article
- Nuclear and cytoplasmic huntingtin inclusions exhibit distinct biochemical composition, interactome and ultrastructural properties.Nature communications · 2021Article
- TFEB Dependent Autophagy-Lysosomal Pathway: An Emerging Pharmacological Target in Sepsis.Frontiers in pharmacology · 2021Review
- Toll-interacting protein impacts on inflammation, autophagy, and vacuole trafficking in human disease.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Protein Trafficking or Cell Signaling: A Dilemma for the Adaptor Protein TOM1.Frontiers in cell and developmental biology · 2021Review
- Toll interacting protein protects bronchial epithelial cells from bleomycin-induced apoptosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Tollip coordinates Parkin-dependent trafficking of mitochondrial-derived vesicles.The EMBO journal · 2020Article
- Phenylbutyrate facilitates homeostasis of non-resolving inflammatory macrophages.Innate immunity · 2020Article
- Editorial: Innate Immunity Programming and Memory in Resolving and Non-Resolving Inflammation.Frontiers in immunology · 2020Article
- Polarization of Low-Grade Inflammatory Monocytes Through TRAM-Mediated Up-Regulation of Keap1 by Super-Low Dose Endotoxin.Frontiers in immunology · 2020Article
- NLRP3 and mTOR Reciprocally Regulate Macrophage Phagolysosome Formation and Acidification AgainstFrontiers in cell and developmental biology · 2020Article
- Macrophage-Specific Hypoxia-Inducible Factor-1α Contributes to Impaired Autophagic Flux in Nonalcoholic Steatohepatitis.Hepatology (Baltimore, Md.) · 2019Article
- Enhanced Neutrophil Immune Homeostasis Due to Deletion of PHLPP.Frontiers in immunology · 2019Article
- Macrophage subsets exhibit distinct E. coli-LPS tolerisable cytokines associated with the negative regulators, IRAK-M and Tollip.PloS one · 2019Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Subclinical super-low-dose endotoxin LPS is a risk factor for the establishment of low-grade inflammation during the pathogenesis and progression of chronic diseases. However, the underlying mechanisms are not well understood. At the cellular level, a disruption of lysosome fusion with endosomes or autophagosomes may contribute to the potentiation of low-grade inflammation. In this study, we identified that subclinical super-low-dose endotoxin LPS can potently inhibit the process of endosome acidification and lysosome fusion with endosomes or autophagosomes in primary macrophages. Super-low-dose LPS induced the inhibitory phosphorylation of VPS34, thus leading to the disruption of endosome-lysosome fusion. This effect may depend upon the clearance and relocation of Tollip in macrophages by super-low-dose LPS. Consistent with this notion, Tollip-deficient macrophages had constitutively elevated levels of VPS34 inhibitory phosphorylation and constitutive disruption of endosome-lysosome fusion. By employing a skin excision wound-healing model, we observed that Tollip-deficient mice had significantly elevated levels of cell stress and reduced wound repair. This study reveals a novel mechanism responsible for the modulation of endosome-lysosome fusion and low-grade inflammation in innate macrophages.
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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.