ArticleCommunications biology2025
Roles of TLR4 in macrophage immunity and macrophage-pulmonary vascular/lymphatic endothelial cell interactions in sepsis.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed.
- Engineered hollow Prussian blue nanoparticles for synergistic anti-inflammatory therapy in sepsis.Materials today. Bio · 2026Article
- Octopus-inspired suction-cup microneedle patch enables intralesional SMAD7/Budesonide co-delivery to disrupt TGF-β-driven fibrotic remodeling.Materials today. Bio · 2026Article
- Metabolic Syndrome-Associated Pulmonary Lipid and Iron Accumulation and Alterations in TLR4/NF-κB Signaling and Ferroptosis-Regulatory Proteins Are Attenuated by Resveratrol Plus Quercetin in Rats.Current issues in molecular biology · 2026Article
- Non-Targeted Metabolomics Profiling and Anti-Inflammatory Potential of Star Anise Extract in Rats with Cold Stress-Aggravated Acute Lung Injury.Metabolites · 2026Article
- ZBP1-driven pyroptosis-associated alveolar macrophages exacerbate epithelial dysfunction in sepsis.Cell death & disease · 2026Article
- Engineering Resatorvid-Loaded Sub-Microgels of Epigallocatechin-3-gallate/Hyaluronic Acid to Treat Acute Lung Injury.Advanced healthcare materials · 2026Article
- Macrophage metabolism reprogramming in sepsis: Pathogenesis and therapeutic implications (Review).International journal of molecular medicine · 2026Review
- A Muribaculaceae-enriched microbiota exacerbates TLR4-dependent Acinetobacter baumannii-induced hyperinflammatory sepsis.Nature communications · 2026Article
- TLR4 promotes ESCC progression by driving inflammation and metabolic reprogramming through SLC39A10-mediated zinc homeostasis.Journal of translational medicine · 2026Article
- Macrophage metabolic reprogramming in sepsis-associated acute lung injury: mechanisms and therapeutic strategies.Frontiers in immunology · 2026Review
- Interleukin-Mediated Macrophage Polarization in Allergic Rhinitis Inflammation: A Systematic Review.Journal of inflammation research · 2026Review
- Differential Modulation of Macrophage Polarization and NF-κB Signaling by Distinct Antibiotics in an in vitro Acute Inflammatory Model.Journal of inflammation research · 2026Article
- Pathogenesis and intervention strategies for metabolic dysfunction-associated fatty liver disease from the perspective of the gut-microbiota-liver axis.Frontiers in immunology · 2026Review
- Extracellular vesicles as emerging platforms for modulating innate immune responses in sepsis-associated acute lung injury.Frontiers in immunology · 2026Review
- A Novel TLR4 Inhibitor DB03476 Rescued Renal Inflammation in Acute Kidney Injury Model.International journal of molecular sciences · 2025Article
- Hexapeptide-Liposome Nanosystem for the Delivery of Endosomal pH Modulator to Treat Acute Lung Injury.Journal of functional biomaterials · 2025Article
- The Role of Toll-like Receptors and Viral Infections in the Pathogenesis and Progression of Pulmonary Arterial Hypertension-A Narrative Review.International journal of molecular sciences · 2025Review
- ADAP-METTL3 modulates the inflammatory responses of macrophages via mCell death & disease · 2025Article
- Immune Dysregulation and Hub Gene Identification in Non-Pulmonary Sepsis-Induced Acute Lung Injury: Insights from Transcriptomic and Experimental Analyses.Current medical science · 2025Article
- Habbe Gule Aakh prevents glycolytic program and alleviates disease progression in a rheumatoid arthritis animal model.Frontiers in immunology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
In sepsis, acute lung injury (ALI) is a severe complication and a leading cause of death, involving complex mechanisms that include cellular and molecular interactions between immune and lung parenchymal cells. In recent decades, the role of Toll-like receptor 4 (TLR4) in mediating infection-induced inflammation has been extensively studied. However, how TLR4 facilitates interactions between innate immune cells and lung parenchymal cells in sepsis remains to be fully understood. This study aims to explore the role of TLR4 in regulating macrophage immunity and metabolism in greater depth. It also seeks to reveal how changes in these processes affect the interaction between macrophages and both pulmonary endothelial cells (ECs) and lymphatic endothelial cells (LECs). Using TLR4 knockout mice and the combined approaches of single-cell RNA sequencing and experimental validation, we demonstrate that in sepsis, TLR4-deficient macrophages upregulate Abca1, enhance cholesterol efflux, and reduce glycolysis, promoting M2 polarization and attenuating inflammation. These metabolic and phenotypic shifts significantly affect their interactions with pulmonary ECs and LECs. Mechanistically, we uncovered that TLR4 operates through multiple pathways in endothelial dysfunction: macrophage TLR4 mediates inflammatory damage to ECs/LECs, while endothelial TLR4 both directly sensitizes cells to lipopolysaccharide-induced injury and determines their susceptibility to macrophage-derived inflammatory signals. These findings reveal the complex role of TLR4 in orchestrating both immune-mediated and direct endothelial responses during sepsis-induced ALI, supporting that targeting TLR4 on multiple cell populations may present an effective therapeutic strategy.
Indexed as
Identifiers
What OpenQuestion holds
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.