ArticleJournal of lipid research2010
ABCA1 promotes the efflux of bacterial LPS from macrophages and accelerates recovery from LPS-induced tolerance.
Article in Journal of lipid research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Cross-talk between lipopolysaccharide tolerance and AGEs in the regulation of macrophage inflammation and cholesterol efflux.Frontiers in immunology · 2026Article
- MicroRNA 223 Enhances ABCA1 Protein Stability and Supports Efflux in Cholesterol-Burdened Macrophages.Cell biochemistry and biophysics · 2025Article
- Lipid metabolism-related genes are involved in the formation of macrophage extracellular traps in allergic airway inflammation.Genes and immunity · 2025Article
- Significance of APOB/APOA1 Ratio in the Prediction of Calcific Aortic Valve Disease.Cardiovascular therapeutics · 2025Article
- Immune and metabolic cross-links in the pathogenesis of comorbid non-alcoholic fatty liver disease.World journal of gastroenterology · 2023Review
- Clinical Significance of Lipid Transport Function of ABC Transporters in the Innate Immune System.Membranes · 2022Review
- Downregulation of Matriptase Inhibits Porphyromonas gingivalis Lipopolysaccharide-Induced Matrix Metalloproteinase-1 and Proinflammatory Cytokines by Suppressing the TLR4/NF-BioMed research international · 2022Article
- Spatiotemporal proteomic profiling of the pro-inflammatory response to lipopolysaccharide in the THP-1 human leukaemia cell line.Nature communications · 2021Article
- Article
- Inflammation-induced foam cell formation in chronic inflammatory disease.Immunology and cell biology · 2015Review
- Acanthoic acid inhibits LPS-induced inflammatory response in human gingival fibroblasts.Inflammation · 2015Article
- Lipopolysaccharides may aggravate apoptosis through accumulation of autophagosomes in alveolar macrophages of human silicosis.Autophagy · 2015Article
- Persistently active microbial molecules prolong innate immune tolerance in vivo.PLoS pathogens · 2013Article
- Molecular mechanisms responsible for the reduced expression of cholesterol transporters from macrophages by low-dose endotoxin.Arteriosclerosis, thrombosis, and vascular biology · 2013Article
- Crosstalk between reverse cholesterol transport and innate immunity.Trends in endocrinology and metabolism: TEM · 2012Review
- Article
- Intracellular lipid flux and membrane microdomains as organizing principles in inflammatory cell signaling.Journal of immunology (Baltimore, Md. : 1950) · 2011Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Macrophages play important roles in both lipid metabolism and innate immunity. We show here that macrophage ATP-binding cassette transporter A1 (ABCA1), a transporter known for its ability to promote apolipoprotein-dependent cholesterol efflux, also participates in the removal of an immunostimulatory bacterial lipid, lipopolysaccharide (LPS). Whereas monocytes require an exogenous lipoprotein acceptor to remove cell-associated LPS, macrophages released LPS in the absence of an exogenous acceptor by a mechanism that was driven, in part, by endogenous apolipoprotein E (apoE). Agents that increased ABCA1 expression increased LPS efflux from wild-type but not ABCA1-deficient macrophages. Preexposure of peritoneal macrophages to LPS for 24 h increased the expression of ABCA1 and increased LPS efflux with a requirement for exogenous apolipoproteins due to suppression of endogenous apoE production. In contrast, LPS preconditioning of ABCA1-deficient macrophages significantly decreased LPS efflux and led to prolonged retention of cell-surface LPS. Although the initial response to LPS was similar in wild-type and ABCA1-deficient macrophages, LPS-induced tolerance was greater and more prolonged in macrophages that lacked ABCA1. Our results define a new role for macrophage ABCA1 in removing cell-associated LPS and restoring normal macrophage responsiveness.
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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.