ArticleJournal of leukocyte biology2016
Role of G-CSF in monophosphoryl lipid A-mediated augmentation of neutrophil functions after burn injury.
Article in Journal of leukocyte biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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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Who cites it
31 citing papers in PubMed, 38 citations in OpenAlex.
- Tissue context as a determinant of trained innate immunity: a conserved molecular toolkit with divergent functional outputs.Journal of leukocyte biology · 2026Review
- GM-CSF ameliorates inflammation from Pseudomonas aeruginosa in a juvenile mouse model of burn injury.Journal of leukocyte biology · 2025Article
- Metabolic adaptations driving innate immune memory: mechanisms and therapeutic implications.Journal of leukocyte biology · 2025Review
- Immunoresponsive gene 1 facilitates TLR4 agonist-induced augmentation of innate antimicrobial immunity.Journal of leukocyte biology · 2025Article
- Role of oxidative stress in post-burn wound healing.Burns & trauma · 2025Review
- Bacteria- and fungus-derived PAMPs induce innate immune memory via similar functional, metabolic, and transcriptional adaptations.Journal of leukocyte biology · 2024Article
- Pretreatment with a novel Toll-like receptor 4 agonist attenuates renal ischemia-reperfusion injury.American journal of physiology. Renal physiology · 2023Article
- Innate Immune Memory and the Host Response to Infection.Journal of immunology (Baltimore, Md. : 1950) · 2022Review
- MyD88-dependent signaling drives toll-like receptor-induced trained immunity in macrophages.Frontiers in immunology · 2022Article
- Neutrophil functional profiling and cytokine augmentation for patients with multiple recurrent infections: A case study.The journal of allergy and clinical immunology. In practice · 2021Article
- A Murine Model of Full-Thickness Scald Burn Injury with Subsequent Wound and Systemic Bacterial Infection.Methods in molecular biology (Clifton, N.J.) · 2021Article
- On the Nonspecific Resistance in Burn Injury: Pathophysiological Aspects (Review).Sovremennye tekhnologii v meditsine · 2021Review
- The role of granulocyte colony‑stimulating factor in breast cancer development: A review.Molecular medicine reports · 2020Review
- Monophosphoryl Lipid a Attenuates Multiorgan Dysfunction During Post-Burn Pseudomonas Aeruginosa Pneumonia in Sheep.Shock (Augusta, Ga.) · 2020Article
- TLR Agonists as Mediators of Trained Immunity: Mechanistic Insight and Immunotherapeutic Potential to Combat Infection.Frontiers in immunology · 2020Review
- The Metabolic Basis of Immune Dysfunction Following Sepsis and Trauma.Frontiers in immunology · 2020Review
- Immune Checkpoints: Novel Therapeutic Targets to Attenuate Sepsis-Induced Immunosuppression.Frontiers in immunology · 2020Review
- Immunobiology and application of toll-like receptor 4 agonists to augment host resistance to infection.Pharmacological research · 2019Review
- Phosphorylated Hexa-Acyl Disaccharides Augment Host Resistance Against Common Nosocomial Pathogens.Critical care medicine · 2019Article
- The TLR4 Agonist Monophosphoryl Lipid A Drives Broad Resistance to Infection via Dynamic Reprogramming of Macrophage Metabolism.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Infection is the leading cause of death in severely burned patients that survive the acute phase of injury. Neutrophils are the first line of defense against infections, but hospitalized burn patients frequently cannot mount an appropriate innate response to infection. Thus, immune therapeutic approaches aimed at improving neutrophil functions after burn injury may be beneficial. Prophylactic treatment with the TLR4 agonist monophosphoryl lipid A is known to augment resistance to infection by enhancing neutrophil recruitment and facilitating bacterial clearance. This study aimed to define mechanisms by which monophosphoryl lipid A treatment improves bacterial clearance and survival in a model of burn-wound sepsis. Burn-injured mice were treated with monophosphoryl lipid A or vehicle, and neutrophil mobilization was evaluated in the presence or absence of Pseudomonas aeruginosa infection. Monophosphoryl lipid A treatment induced significant mobilization of neutrophils from the bone marrow into the blood and sites of infection. Neutrophil mobilization was associated with decreased bone marrow neutrophil CXCR4 expression and increased plasma G-CSF concentrations. Neutralization of G-CSF before monophosphoryl lipid A administration blocked monophosphoryl lipid A-induced expansion of bone marrow myeloid progenitors and mobilization of neutrophils into the blood and their recruitment to the site of infection. G-CSF neutralization ablated the enhanced bacterial clearance and survival benefit endowed by monophosphoryl lipid A in burn-wound-infected mice. Our findings provide convincing evidence that monophosphoryl lipid A-induced G-CSF facilitates early expansion, mobilization, and recruitment of neutrophils to the site of infection after burn injury, allowing for a robust immune response to infection.
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