ArticleInfection and immunity2005
Endotoxin priming improves clearance of Pseudomonas aeruginosa in wild-type and interleukin-10 knockout mice.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 49 citations in OpenAlex.
- Pre-existing systemic inflammation impairs bacterial clearance in the spleen.Intensive care medicine experimental · 2026Article
- Monophosphoryl lipid A boosts macrophage antimicrobial immunity by metabolically regulating source-specific ROS generation.Frontiers in immunology · 2026Article
- Review
- Metabolic adaptations driving innate immune memory: mechanisms and therapeutic implications.Journal of leukocyte biology · 2025Review
- Neutrophils and galectin-3 defend mice from lethal bacterial infection and humans from acute respiratory failure.Nature communications · 2024Article
- Innate Immune Memory and the Host Response to Infection.Journal of immunology (Baltimore, Md. : 1950) · 2022Review
- A transient increase in MHC-IIVeterinary research · 2020Article
- The Metabolic Basis of Immune Dysfunction Following Sepsis and Trauma.Frontiers in immunology · 2020Review
- TLR Agonists as Mediators of Trained Immunity: Mechanistic Insight and Immunotherapeutic Potential to Combat Infection.Frontiers in immunology · 2020Review
- Immunobiology and application of toll-like receptor 4 agonists to augment host resistance to infection.Pharmacological research · 2019Review
- The impact of the systemic inflammatory response on hepatic bacterial elimination in experimental abdominal sepsis.Intensive care medicine experimental · 2019Article
- MicroRNA-Mediated Control of Inflammation and Tolerance in Pregnancy.Frontiers in immunology · 2019Review
- Septic predictor index: A novel platform to identify thermally injured patients susceptible to sepsis.Surgery · 2018Article
- Precision Immunotherapy for Sepsis.Frontiers in immunology · 2018Review
- Comparative Transcriptome Profiles of Human Blood in Response to the Toll-like Receptor 4 Ligands Lipopolysaccharide and Monophosphoryl Lipid A.Scientific reports · 2017Article
- Decreased Risk of Ventilator-Associated Pneumonia in Sepsis Due to Intra-Abdominal Infection.PloS one · 2015Observational
- The immunobiology of toll-like receptor 4 agonists: from endotoxin tolerance to immunoadjuvants.Shock (Augusta, Ga.) · 2013Review
- Targeting toll-like receptor signaling as a novel approach to prevent ocular infectious diseases.The Indian journal of medical research · 2013Review
- Period of irreversible therapeutic intervention during sepsis correlates with phase of innate immune dysfunction.The Journal of biological chemistry · 2012Article
- Toll-like receptor 2 ligand pretreatment attenuates retinal microglial inflammatory response but enhances phagocytic activity toward Staphylococcus aureus.Infection and immunity · 2012Article
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 at 1 institution in 1 country.
Funding
Abstract
Endotoxin (lipopolysaccharide [LPS]) tolerance is an altered state of immunity caused by prior exposure to LPS, in which production of many cytokines, including gamma interferon (IFN-gamma) and interleukin-12 (IL-12), are reduced but secretion of the anti-inflammatory cytokine IL-10 is increased in response to a subsequent LPS challenge. This pattern of cytokine production is also characteristic of postinflammatory immunosuppression. Therefore, we hypothesized that LPS-primed mice would exhibit an impaired ability to respond to systemic infection with the opportunistic pathogen Pseudomonas aeruginosa. We further hypothesized that depletion of IL-10 would reverse the endotoxin-tolerant state. To test this hypothesis, systemic clearance of Pseudomonas aeruginosa was measured for LPS-primed wild-type and IL-10-deficient mice. LPS-primed wild-type mice exhibited significant suppression of LPS-induced IFN-gamma and IL-12 but increased IL-10 production in blood and spleen compared to levels exhibited by saline-primed wild-type mice. The suppressed production of IFN-gamma and IL-12 caused by LPS priming was ablated in the spleens, but not blood, of IL-10 knockout mice. LPS-primed wild-type mice cleared Pseudomonas aeruginosa from lungs and blood more effectively than saline-primed mice. LPS-primed IL-10-deficient mice were particularly efficient in clearing Pseudomonas aeruginosa after systemic challenge. These studies show that induction of LPS tolerance enhanced systemic clearance of Pseudomonas aeruginosa and that this effect was augmented by neutralization of IL-10.
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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.