ArticlePLoS pathogens2017
Acyloxyacyl hydrolase promotes the resolution of lipopolysaccharide-induced acute lung injury.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 59 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
- Engineering a T7 bacteriophage to attenuate LPS-driven inflammatory responses during bacteriolysis.Applied and environmental microbiology · 2026Article
- Histone H3 lysine 9 tri-methylation is associated with pterygium.BMC ophthalmology · 2025Article
- Oral administration of Lactobacillus plantarum expressing aCD11c modulates cellular immunity alleviating inflammatory injury due to Klebsiella pneumoniae infection.BMC veterinary research · 2024Article
- Acyloxyacyl Hydrolase Protects against Kidney Injury via Inhibition of Tubular CD74-Macrophage Crosstalk.International journal of biological sciences · 2024Article
- Intravenous BCG vaccination reduces SARS-CoV-2 severity and promotes extensive reprogramming of lung immune cells.iScience · 2023Article
- Liver and Muscle Transcriptomes Differ in Mid-Lactation Cows Divergent in Feed Efficiency in the Presence or Absence of Supplemental Rumen-Protected Choline.Metabolites · 2023Article
- In Situ Neutralization and Detoxification of LPS to Attenuate Hyperinflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Acyloxyacyl hydrolase promotes pulmonary defense by preventing alveolar macrophage tolerance.PLoS pathogens · 2023Article
- The leaky gut and the gut microbiome in sepsis - targets in research and treatment.Clinical science (London, England : 1979) · 2023Article
- Bifidobacterium longum supplementation improves age-related delays in fracture repair.Aging cell · 2023Article
- Acyloxyacyl hydrolase deficiency induces chronic inflammation and bone loss in male mice.Journal of molecular medicine (Berlin, Germany) · 2022Article
- Carboxylesterase 1d Inactivation Augments Lung Inflammation in Mice.ACS pharmacology & translational science · 2022Article
- Periodontitis and cardiometabolic disorders: The role of lipopolysaccharide and endotoxemia.Periodontology 2000 · 2022Review
- Effects of Human RelA Transgene on Murine Macrophage Inflammatory Responses.Biomedicines · 2022Article
- Dynamic single-cell RNA sequencing reveals BCG vaccination curtails SARS-CoV-2 induced disease severity and lung inflammation.bioRxiv : the preprint server for biology · 2022Article
- Article
- The Reaction Pathway of miR-30c-5p Activates Lipopolysaccharide Promoting the Course of Traumatic and Hemorrhagic Shock Acute Lung Injury.BioMed research international · 2022Article
- Time-Course Transcriptome Analysis of Lungs From Mice Infected With HypervirulentFrontiers in cellular and infection microbiology · 2022Article
- Bioinformatics and systems-biology analysis to determine the effects of Coronavirus disease 2019 on patients with allergic asthma.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary infection is the most common risk factor for acute lung injury (ALI). Innate immune responses induced by Microbe-Associated Molecular Pattern (MAMP) molecules are essential for lung defense but can lead to tissue injury. Little is known about how MAMP molecules are degraded in the lung or how MAMP degradation/inactivation helps prevent or ameliorate the harmful inflammation that produces ALI. Acyloxyacyl hydrolase (AOAH) is a host lipase that inactivates Gram-negative bacterial endotoxin (lipopolysaccharide, or LPS). We report here that alveolar macrophages increase AOAH expression upon exposure to LPS and that Aoah+/+ mice recover more rapidly than do Aoah-/- mice from ALI induced by nasally instilled LPS or Klebsiella pneumoniae. Aoah-/- mouse lungs had more prolonged leukocyte infiltration, greater pro- and anti-inflammatory cytokine expression, and longer-lasting alveolar barrier damage. We also describe evidence that the persistently bioactive LPS in Aoah-/- alveoli can stimulate alveolar macrophages directly and epithelial cells indirectly to produce chemoattractants that recruit neutrophils to the lung and may prevent their clearance. Distinct from the prolonged tolerance observed in LPS-exposed Aoah-/- peritoneal macrophages, alveolar macrophages that lacked AOAH maintained or increased their responses to bioactive LPS and sustained inflammation. Inactivation of LPS by AOAH is a previously unappreciated mechanism for promoting resolution of pulmonary inflammation/injury induced by Gram-negative bacterial infection.
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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.