ArticleCell death & disease2018
Low doses of LPS exacerbate the inflammatory response and trigger death on TLR3-primed human monocytes.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.
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Who cites it
40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 57 citations in OpenAlex.
- The relation between the gut microbiome and osteoarthritis: A systematic review of literature.PloS one · 2021Pooled it
- Immune capacity determines outcome following surgery or trauma: a systematic review and meta-analysis.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2020Pooled it
- A novel two-hit murine model of viral-primed sepsis-associated acute kidney injury.American journal of physiology. Renal physiology · 2026Article
- Investigation ofVeterinary sciences · 2026Article
- Single-cell RNA sequencing reveals multiple pathways involving pulmonary immune and epithelial cells through which aryl hydrocarbon receptor activation attenuates acute respiratory distress syndrome.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- A distinct monocyte transcriptional state links systemic immune dysregulation to pulmonary impairment in long COVID.Nature immunology · 2026Article
- The Clinical View of Sepsis-Associated AKI: How Basic Science Can Help Solve This Problem.Seminars in nephrology · 2025Review
- Nanofibrous dressings incorporating a synergistic antibacterial-anti-inflammatory effect for infected wound healing.Materials today. Bio · 2025Article
- Time-resolved monitoring of yeast responses to lipopolysaccharide exposure by cell-released volatile organic compounds.Applied and environmental microbiology · 2025Article
- Effect of a Gluten-Free Diet on the Intestinal Microbiota of Women with Celiac Disease.Antibiotics (Basel, Switzerland) · 2025Article
- Liposomal Nanotraps NeutralizeInfectious microbes & diseases · 2025Article
- NEDD4 E3 ligase-catalyzed NAMPT ubiquitination and autophagy activation are essential for pyroptosis-independent NAMPT secretion in human monocytes.Cell communication and signaling : CCS · 2025Article
- Decoding Sepsis: Unraveling Key Signaling Pathways for Targeted Therapies.Research (Washington, D.C.) · 2025Review
- Cell- and Serum-Derived Proteins Act as DAMPs to Activate RAW 264.7 Macrophage-like Cells on Silicone Implants.ACS biomaterials science & engineering · 2024Article
- Distribution patterns and influential factors of pathogenic bacteria in freshwater aquaculture sediments.Environmental science and pollution research international · 2024Article
- Unravelling the mechanisms causing murepavadin resistance inFrontiers in cellular and infection microbiology · 2024Article
- Processing stimulus dynamics by the NF-κB network in single cells.Experimental & molecular medicine · 2023Review
- Monocyte regulation by gut microbial signals.Trends in microbiology · 2023Review
- High-Dose Vitamin B6 (Pyridoxine) Displays Strong Anti-Inflammatory Properties in Lipopolysaccharide-Stimulated Monocytes.Biomedicines · 2023Article
- Inflammatory macrophage to hepatocyte signals can be prevented by extracellular vesicle reprogramming.Journal of cell science · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TLR sensing of pathogens triggers monocyte activation to initiate the host innate immune response to infection. Monocytes can dynamically adapt to different TLR agonists inducing different patterns of inflammatory response, and the sequence of exposure to TLRs can dramatically modulate cell activation. Understanding the interactions between TLR signalling that lead to synergy, priming and tolerance to TLR agonists may help explain how prior infections and inflammatory conditioning can regulate the innate immune response to subsequent infections. Our goal was to investigate the role of MyD88-independent/dependent TLR priming on modulating the monocyte response to LPS exposure. We stimulated human blood monocytes with agonists for TLR4 (LPS), TLR3 (poly(I:C)) and TLR7/8 (R848) and subsequently challenged them to low doses of endotoxin. The different TLR agonists promoted distinct inflammatory signatures in monocytes. Upon subsequent LPS challenge, LPS- and R848-primed monocytes did not enhance the previous response, whereas poly(I:C)-primed monocytes exhibited a significant inflammatory response concomitant with a sharp reduction on cell viability. Our results show that TLR3-primed monocytes are prompted to cell death by apoptosis in the presence of low endotoxin levels, concurrent with the production of high levels of TNFα and IL6. Of note, blocking of TNFR I/II in those monocytes did reduce TNFα production but did not abrogate cell death. Instead, direct signalling through TLR4 was responsible of such effect. Collectively, our study provides new insights on the effects of cross-priming and synergism between TLR3 and TLR4, identifying the selective induction of apoptosis as a strategy for TLR-mediated host innate response.
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