ArticlePLoS pathogens2013
Persistently active microbial molecules prolong innate immune tolerance in vivo.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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
23 citing papers in PubMed, 41 citations in OpenAlex.
- Acyloxyacyl Hydrolase-Mediated Lipopolysaccharide Inactivation Limits Macrophage Endotoxin Tolerance and Promotes Inflammation and Fibrosis in Metabolic Dysfunction-Associated Steatohepatitis.Cellular and molecular gastroenterology and hepatology · 2026Article
- Targeting the mevalonate pathway potentiates NUAK1 inhibition-induced immunogenic cell death and antitumor immunity.Cell reports. Medicine · 2025Article
- Acyloxyacyl Hydrolase Protects against Kidney Injury via Inhibition of Tubular CD74-Macrophage Crosstalk.International journal of biological sciences · 2024Article
- Article
- Acyloxyacyl hydrolase promotes pulmonary defense by preventing alveolar macrophage tolerance.PLoS pathogens · 2023Article
- Acyloxyacyl hydrolase deficiency induces chronic inflammation and bone loss in male mice.Journal of molecular medicine (Berlin, Germany) · 2022Article
- Vaginal neutrophil infiltration is contingent on ovarian cycle phase and independent of pathogen infection.Frontiers in immunology · 2022Article
- A highly conserved host lipase deacylates oxidized phospholipids and ameliorates acute lung injury in mice.eLife · 2021Article
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- SIDT1-dependent absorption in the stomach mediates host uptake of dietary and orally administered microRNAs.Cell research · 2021Article
- Effects of 17β-Estradiol on Monocyte/Macrophage Response toFrontiers in cellular and infection microbiology · 2021Article
- Biochemical transformation of bacterial lipopolysaccharides by acyloxyacyl hydrolase reduces host injury and promotes recovery.The Journal of biological chemistry · 2020Review
- Dynamin-related Irgm proteins modulate LPS-induced caspase-11 activation and septic shock.EMBO reports · 2020Article
- LPS inactivation by a host lipase allows lung epithelial cell sensitization for allergic asthma.The Journal of experimental medicine · 2018Article
- Crystal structure of the mammalian lipopolysaccharide detoxifier.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Acyloxyacyl hydrolase promotes the resolution of lipopolysaccharide-induced acute lung injury.PLoS pathogens · 2017Article
- PPE38 Protein ofFrontiers in cellular and infection microbiology · 2017Article
- Endotoxemia-menace, marker, or mistake?Journal of leukocyte biology · 2016Review
- Modulation of inflammatory response of wounds by antimicrobial photodynamic therapy.Laser therapy · 2015Article
- Ascites bacterial burden and immune cell profile are associated with poor clinical outcomes in the absence of overt infection.PloS one · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Measures that bolster the resolution phase of infectious diseases may offer new opportunities for improving outcome. Here we show that inactivation of microbial lipopolysaccharides (LPS) can be required for animals to recover from the innate immune tolerance that follows exposure to Gram-negative bacteria. When wildtype mice are exposed to small parenteral doses of LPS or Gram-negative bacteria, their macrophages become reprogrammed (tolerant) for a few days before they resume normal function. Mice that are unable to inactivate LPS, in contrast, remain tolerant for several months; during this time they respond sluggishly to Gram-negative bacterial challenge, with high mortality. We show here that prolonged macrophage reprogramming is maintained in vivo by the persistence of stimulatory LPS molecules within the cells' in vivo environment, where naïve cells can acquire LPS via cell-cell contact or from the extracellular fluid. The findings provide strong evidence that inactivation of a stimulatory microbial molecule can be required for animals to regain immune homeostasis following parenteral exposure to bacteria. Measures that disable microbial molecules might enhance resolution of tissue inflammation and help restore innate defenses in individuals recovering from many different infectious diseases.
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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.