ArticleProstaglandins & other lipid mediators2015
Lipopolysaccharide suppresses carboxylesterase 2g activity and 2-arachidonoylglycerol hydrolysis: A possible mechanism to regulate inflammation.
Article in Prostaglandins & other lipid mediators, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 29 citations in OpenAlex.
- Proteomic profiling reveals immunologic mediators of endotoxin-related lung function decline: a longitudinal prospective study in textile workers.Respiratory research · 2026Article
- Effects of incubation with endocannabinoids on the expression of endocannabinoid and inflammatory components following an ex vivo lipopolysaccharide challenge in leukocytes of dairy cows.JDS communications · 2026Article
- JZL-184 Alleviate Neurological Impairment through Regulation of Mitochondrial Transfer and Lipid Droplet Accumulation after Cardiac Arrest.Molecular neurobiology · 2025Article
- Carboxylesterase 1-mediated endocannabinoid metabolism in skin: role in melanoma progression in BRafCancer & metabolism · 2025Article
- Analysis of fatty acid-derived lipids in critically ill patients after cardiac surgery yields novel pathophysiologically relevant mediators with possible relevance for systemic inflammatory reactions.Frontiers in immunology · 2024Article
- Cnr1Chemico-biological interactions · 2023Article
- Inhibiting degradation of 2-arachidonoylglycerol as a therapeutic strategy for neurodegenerative diseases.Pharmacology & therapeutics · 2023Review
- Carboxylesterase 1d Inactivation Augments Lung Inflammation in Mice.ACS pharmacology & translational science · 2022Article
- Proteomic and phosphorylated proteomic landscape of injured lung in juvenile septic rats with therapeutic application of umbilical cord mesenchymal stem cells.Frontiers in immunology · 2022Article
- Effects of Chlorpyrifos on Serine Hydrolase Activities, Lipid Mediators, and Immune Responses in Lungs of Neonatal and Adult Mice.Chemical research in toxicology · 2021Article
- Pig Liver Esterases Hydrolyze Endocannabinoids and Promote Inflammatory Response.Frontiers in immunology · 2021Article
- Effects of the monoacylglycerol lipase inhibitor JZL184 on chickens infected with avian pathogenicCanadian journal of veterinary research = Revue canadienne de recherche veterinaire · 2020Article
- Differential Thermoregulatory and Inflammatory Patterns in the Circadian Response to LPS-Induced Septic Shock.Frontiers in cellular and infection microbiology · 2020Article
- Characterization of Endocannabinoid-Metabolizing Enzymes in Human Peripheral Blood Mononuclear Cells under Inflammatory Conditions.Molecules (Basel, Switzerland) · 2018Article
- Endocannabinoid hydrolases in avian HD11 macrophages identified by chemoproteomics: inactivation by small-molecule inhibitors and pathogen-induced downregulation of their activity.Molecular and cellular biochemistry · 2018Article
- Carboxylesterases in lipid metabolism: from mouse to human.Protein & cell · 2018Review
- Circulating Endocannabinoids: From Whence Do They Come and Where are They Going?Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Review
- Interaction between Cannabinoid System and Toll-Like Receptors Controls Inflammation.Mediators of inflammation · 2016Review
- Inhibition of Endocannabinoid-Metabolizing Enzymes in Peripheral Tissues Following Developmental Chlorpyrifos Exposure in Rats.International journal of toxicologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Inflammation is an important part of the innate immune response and is involved in the healing of many disease processes; however, chronic inflammation is a harmful component of many diseases. The regulatory mechanisms of inflammation are incompletely understood. One possible regulatory mechanism is the endocannabinoid system. Endocannabinoids such as 2-arachidonoylglycerol (2-AG) and anandamide (AEA) are generally anti-inflammatory via engagement of the cannabinoid receptor 2 (CB2) on innate cells; therefore, preventing the degradation of endocannabinoids by specific serine hydrolases such as fatty acid amide hydrolase (FAAH), monoacylglycerol lipase (MAGL), and carboxylesterases (CES) might decrease inflammation. We hypothesized that the activities of these catabolic enzymes would decrease with a subsequent increase in 2-AG and AEA in a model of inflammation. Mice were injected with lipopolysaccharide (LPS) for 6 or 24h, and inflammation was confirmed by an increase in interleukin-6 (il6) and il17 gene expression. Activity-based protein profiling (ABPP) of serine hydrolases showed no significant difference in various serine hydrolase activities in brain or liver, whereas a modest decrease in Ces activity in spleen after LPS administration was noted. 2-AG hydrolase activity in the spleen was also decreased at 6h post LPS, which was corroborated by LPS treatment of splenocytes ex vivo. ABPP-MudPIT proteomic analysis suggested that the decreased 2-AG hydrolysis in spleen was due to a reduction in Ces2g activity. These studies suggest that the endocannabinoid system could be activated via suppression of a 2-AG catabolic enzyme in response to inflammatory stimuli as one mechanism to limit inflammation.
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.