ArticleThe Journal of biological chemistry2013
Molecular mechanism responsible for the priming of macrophage activation.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 130 citations in OpenAlex.
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- Detection of Microbial Contamination in Nanomaterials Using LAL, rFC and Cell-Based Assays: Implications for Nanotoxicological Hazard Assessment.Nanomaterials (Basel, Switzerland) · 2025Article
- Myeloid GPSM1 regulates atherosclerosis progression by governing monocyte and macrophage activation and chemotaxis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Hematopoietic stem cell state and fate in trained immunity.Cell communication and signaling : CCS · 2025Review
- Repeated and alternate stimulations with dsRNA and SEB alter responses in macrophages and epithelial cells.The World Allergy Organization journal · 2025Article
- Oral and transdermal administration of lipopolysaccharide safely enhances self-healing ability through the macrophage network.Frontiers in immunology · 2025Review
- Short-term heavy drinking in a non-human primate model skews monocytes toward a hypo-inflammatory phenotype.Frontiers in immunology · 2025Article
- Recent Advances of Trained immunity in Macrophages.International journal of biological sciences · 2025Review
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- Maintenance of homeostasis by TLR4 ligands.Frontiers in immunology · 2024Review
- High mobility group box protein 1 sensitizes mononuclear cells to further contact with lipopolysaccharide.Central-European journal of immunology · 2024Article
- Prolonged Inhibition of the MEK1/2-ERK Signaling Axis Primes Interleukin-1 Beta Expression through Histone 3 Lysine 9 Demethylation in Murine Macrophages.International journal of molecular sciences · 2023Article
- Utility of In Vitro Cellular Models of Low-Dose Lipopolysaccharide in Elucidating the Mechanisms of Anti-Inflammatory and Wound-Healing-Promoting Effects of Lipopolysaccharide Administration In Vivo.International journal of molecular sciences · 2023Review
- Training vs. Tolerance: The Yin/Yang of the Innate Immune System.Biomedicines · 2023Review
- Anti-inflammatory and anti-fibrotic effects of berberine-loaded liquid crystalline nanoparticles.EXCLI journal · 2023Article
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- Immunomodulatory role of oral microbiota in inflammatory diseases and allergic conditions.Frontiers in allergy · 2023Review
- Cochlear implant material effects on inflammatory cell function and foreign body response.Hearing research · 2022Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Host macrophages can be preprogrammed into opposing primed or tolerant states depending upon the nature and quantities of external stimulants. The paradigm of priming and tolerance has significant implications in the pathogenesis and resolution of both acute and chronic inflammatory diseases. However, the responsible mechanisms are not well understood. Here, we report that super low dose bacterial endotoxin lipopolysaccharide (LPS), as low as 5 pg/ml, primes the expression of proinflammatory mediators in macrophages upon a second high dose LPS challenge (100 ng/ml), although 5 pg/ml LPS itself does not trigger noticeable macrophage activation. Mice primed with super low dose LPS (0.5 μg/kg body weight) in vivo experience significantly elevated mortality following a second hit of high dose LPS as compared with saline-primed control mice. Mechanistically, we demonstrate that LPS primes macrophages by removing transcriptional suppressive RelB through interleukin receptor-associated kinase 1 and Tollip (Toll-interacting protein)-dependent mechanisms. This is in sharp contrast to the well documented RelB stabilization and induction by high dose LPS, potentially through the phosphoinositide 3-kinase (PI3K) pathway. Super low dose and high dose LPS cause opposing modulation of interleukin receptor-associated kinase 1 and PI3K pathways and lead to opposing regulation of RelB. The pathway switching induced by super low versus high dose LPS underscores the importance of competing intracellular circuitry during the establishment of macrophage priming and tolerance.
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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.