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30 results for “EICOSANOIDS”
Data from: Crystalline silica-induced proinflammatory eicosanoid storm in novel alveolar macrophage model quelled by docosahexaenoic acid
<p>Introduction: Workplace exposure to respirable crystalline silica (cSiO<sub>2</sub>) is associated with chronic inflammatory and autoimmune diseases. At the mechanistic level, cSiO<sub>2</sub> particles are quickly phagocytosed by resident alveolar macrophages (AMs) in the lung, causing a robust cycle of proinflammatory cytokine release, lysosomal rupture, mitochondrial toxicity, and immunogenic cell death if the particle is not efficiently cleared by the lung. We and others have demonstrated in bone marrow-derived and transformed macrophage models that supplementation with the ω-3 polyunsaturated fatty acid (PUFA) docosahexaenoic acid (DHA) contributes to increased membrane phospholipid content of DHA and subsequent suppression of cSiO<sub>2</sub>-triggered inflammatory responses. However, mechanistic exploration of ω-3 PUFA effects in AMs is challenging due to reliance on short-lived primary AMs derived from lung lavage fluid.</p> <p>Methods: To address these limitations, we have employed a recently developed novel self-renewing AM model from C57BL/6 mice, fetal liver-derived alveolar-like macrophages (FLAMs), that is phenotypically representative of primary lung AM populations. We found that incubation of FLAMs with 25 µM DHA as ethanolic suspensions or as complexes with bovine serum albumin were equally effective at increasing ω-3 PUFA content of phospholipids at the expense of the ω-6 PUFA arachidonic acid (ARA) and the ω-9 monounsaturated fatty acid oleic acid. Based on these findings, FLAMs were treated with 25 µM DHA in EtOH or EtOH vehicle (VEH) for 24 h, with or without LPS for 2 h, and with or without cSiO<sub>2</sub> for 1.5 or 4 h then proinflammatory cytokine release, lysosomal membrane permeabilization, and mitochondrial depolarization assessed. In addition, oxylipin metabolites were measured using a targeted LC-MS lipidomics panel of 156 metabolites.</p> <p>Results: Regardless of whether FLAMs were LPS-primed, cSiO<sub>2</sub>-triggered lysosomal permeability, mitochondrial toxicity, and cell death were not impacted by DHA. LPS+cSiO<sub>2</sub> elicited marked IL-1α, IL-1β, and TNF-α release after 1.5 and 4 h of cSiO<sub>2</sub> exposure, which was significantly inhibited by DHA. In VEH-treated cells, cSiO<sub>2</sub> alone and LPS+cSiO2 induced synthesis of ARA-derived proinflammatory oxylipins including prostaglandins, leukotrienes, and thromboxanes that was suppressed by DHA. In addition, DHA promoted synthesis of pro-resolving DHA-derived oxylipins at the expense of ARA-derived oxylipins.</p> <p>Discussion: FLAMs were amenable to lipidome modulation by DHA, which suppressed cSiO<sub>2</sub>-triggered proinflammatory cytokine responses and ARA-derived oxylipins that potentially contribute to the particle's toxicity in the lung. FLAMs are a promising in vitro alternative to primary AMs for investigating interventions against toxicant-triggered inflammation and autoimmunity in the lung.</p>
Dietary Fat, Eicosanoids and Breast Cancer Risk
ClinicalTrials.gov study NCT01824498. IPD Sharing: Not stated. Countries: 1. Publications: 4.
Data from: Crystalline silica-induced proinflammatory eicosanoid storm in novel alveolar macrophage model quelled by docosahexaenoic acid
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Data from: Early mechanistic events induced by low molecular weight polycyclic aromatic hydrocarbons in mouse lung epithelial cells: a role for eicosanoid signaling
Low molecular weight polycyclic aromatic hydrocarbons (LMW PAHs; <206.3 g/mol) are under regulated environmental contaminants (e.g., secondhand smoke) that lead to gap junction dysregulation, p38 MAPK activation, and increased mRNA production of inflammatory mediators, such as cytokines and cyclooxygenase (COX2), in lung epithelial cells. However, the early mechanisms involving lipid signaling through the arachidonic acid pathway and subsequent eicosanoid production leading to these downstream events are not known. Common human exposures are to mixtures of LMW PAH's, thus C10 cells (a mouse lung epithelial cell line) were exposed to a representative binary PAH mixture, 1-methylanthracene (1-MeA) and fluoranthene (Flthn), for 30 min – 24 h with and without p38 and cytosolic phospholipase A2 (cPLA2) inhibitors. cPLA2 inhibition reversed PAH-induced phospho-p38 MAPK activation and gap junction dysregulation at 30 min. A significant biphasic increase of cPLA2 protein was observed at 30 min, 2, & 4 h, as well as COX2 protein at 2 & 8 h. Untargeted metabolomics demonstrated a similar trend with significantly changing metabolites at 30 min & 4 h of exposure relative to 1 h; a "cPLA2-like" subset of metabolites within the biphasic response were predominately phospholipids. argeted metabolomics showed several eicosanoids (e.g., prostaglandin D2 (PGD2), PGE2α) were significantly increased at 4, 8, and 12 h following exposure to the binary PAH mixture and this effect was p38-dependent. Lastly, PAH metabolism was not observed until after 8 h. These results indicate an early lipid signaling mechanism of PAH toxicity in lung epithelial cells due to parent PAH compounds.
Study of the Effect of Eicosanoids on Contractile Activity of Pregnant Human Myometrium in Pathological Situation
ClinicalTrials.gov study NCT00939744. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Eicosanoids in Human Heart Failure
ClinicalTrials.gov study NCT05305170. IPD Sharing: UNDECIDED. Countries: 1. Publications: 12.
The Role of Eicosanoids in the Cardiovascular Actions of Inhaled Nanoparticles
ClinicalTrials.gov study NCT03659864. IPD Sharing: NO. Countries: 1. Publications: 1.
Effect of Packed Red Blood Cell Transfusion on Eicosanoid Profiles in Plasma of Intensive Care Patients
ClinicalTrials.gov study NCT03782623. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
Place of Circulating Biomarkers and Respiratory Eicosanoids in the Prognosis of Severe Forms of Covid-19 Pneumonia
ClinicalTrials.gov study NCT04485364. IPD Sharing: Not stated. Countries: 1. Publications: 4.
Data from: Early mechanistic events induced by low molecular weight polycyclic aromatic hydrocarbons in mouse lung epithelial cells: a role for eicosanoid signaling
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Pathways of Eicosanoid Metabolism
ClinicalTrials.gov study NCT04464070. IPD Sharing: YES. Countries: 1. Publications: 0.
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) Alters Hepatic Polyunsaturated Fatty Acid Metabolism and Eicosanoid Biosynthesis in Female Sprague-Dawley Rats
GEO Series GSE110294. Rattus norvegicus. 34 samples. Type: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing.
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) Alters Hepatic Polyunsaturated Fatty Acid Metabolism and Eicosanoid Biosynthesis in Female Sprague-Dawley Rats [RNA-Seq]
GEO Series GSE110293. Rattus norvegicus. 24 samples. Type: Expression profiling by high throughput sequencing.
PLCG2 regulates endocannabinoid and eicosanoid networks in innate immune cells
GEO Series GSE180274. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
Cytokine and Eicosanoid Mediators in Coronavirus Disease 2019 (COVID-19)
ClinicalTrials.gov study NCT04452942. IPD Sharing: NO. Countries: 1. Publications: 0.
Effects of Lumiracoxib and Ibuprofen on Blood Pressure and Urinary Eicosanoid Excretion in Osteoarthritis Patients With Controlled Hypertension
ClinicalTrials.gov study NCT00419796. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Eicosanoid Lipids by Airway Cells During Infection With Human Rhinoviruses
ClinicalTrials.gov study NCT01898767. IPD Sharing: YES. Countries: 1. Publications: 0.
RNA-seq analysis reveals endogenous aryl hydrocarbon receptor regulation is highly associated with eicosanoid synthesis and tumor necrosis factor activity in MCF-7 cancer cells
GEO Series GSE52036. Homo sapiens. 11 samples. Type: Expression profiling by high throughput sequencing.
Inhibition of Eicosanoid Degradation Mitigates Fibrosis of the Heart
GEO Series GSE217957. Rattus norvegicus. 16 samples. Type: Expression profiling by high throughput sequencing.
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) Alters Hepatic Polyunsaturated Fatty Acid Metabolism and Eicosanoid Biosynthesis in Female Sprague-Dawley Rats [ChIP-Seq]
GEO Series GSE110282. Rattus norvegicus. 10 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
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