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84 results for “docosahexaenoic acid”
Fig 2 in Docosahexaenoic Acid (DHA) Reduces LPSInduced Inflammatory Response Via ATF3 Transcription Factor and Stimulates Src/ Syk Signaling-Dependent Phagocytosis in Microglia
<p>Proteome profiler arrays (A and B) and expression of ATF3 gene (C) in microglia. Representative array membranes (A) and the relative levels of cytokines and chemokines (B) in microglia preincubated with 20 μM DHA and next treated with 10 ng/ml LPS.</p>
Fig 1 in Docosahexaenoic Acid (DHA) Reduces LPSInduced Inflammatory Response Via ATF3 Transcription Factor and Stimulates Src/ Syk Signaling-Dependent Phagocytosis in Microglia
<p>Viability of microglia incubated with various concentration of DHA for 12 h (A) and LPS for 2.5 h (B). Viability of microglia incubated with 20 μM DHA followed by 10 ng/ ml LPS treatment (C).</p>
Data from: Docosahexaenoic acid intake suppresses acute silica-induced inflammation, autoantibody production, and autoimmune-related gene expression in lupus-prone mice
<p class="MsoNormal">Short-term repeated intranasal exposure crystalline silica (cSiO<sub>2</sub>), a known human autoimmune trigger, induces uncontrolled inflammation, upregulated IFN-stimulated gene expression, diverse autoantibody production, and glomerulonephritis in lupus-prone female NZBWF1 mice. Dietary supplementation with the omega-3 fatty acid docosahexaenoic acid (DHA) prevents subchronic cSiO<sub>2</sub> triggering of these lupus hallmarks. To understand how this intervention impacts acute effects of cSiO<sub>2</sub>, we fed NZBWF1 mice control (CON) or DHA-containing diet, subjected them to a single acute intranasal instillation of 2.5 mg cSiO<sub>2</sub>, then compared pulmonary inflammatory/autoimmune responses and autoimmune-related gene expression in experimental cohorts terminated at 7 and 28 d post-instillation (PI). Acute cSiO<sub>2 </sub>exposure of CON-fed mice elicited decreased macrophage and increased neutrophil numbers at 7 d PI, whereas at 28 d PI, CON-fed mice treated with particle displayed elevated total cell, macrophage, neutrophil, and lymphocyte counts. In contrast, DHA-fed mice treated with cSiO<sub>2</sub> exhibited less macrophage loss at 7 d PI and reduced total cell, macrophage, and lymphocyte accumulation at 28 d PI. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) of lung sections suggested that cSiO<sub>2</sub> induced more robust cell death at 7 d PI in CON-fed than DHA-fed mice. Targeted multiplex ELISA of lung extracts showed that at 28 d PI, cSiO<sub>2</sub> induced higher concentrations of inflammation-associated cytokines (IL-1α, IL-6, and GM-CSF) and IFN-stimulated chemokines (CCL2, CCL3, CXCL10) in the CON-fed cohort than in the DHA-fed cohort. Autoantigen protein microarray of BALF collected at 28 d PI indicated that cSiO<sub>2</sub> induced higher autoantibody responses for representative nuclear, ribosomal, mitochondrial, and complement proteins in CON-fed mice than DHA-fed mice. Gene expression analyses with NanoString Autoimmune Gene Expression assay revealed greater cSiO<sub>2</sub>-triggered upregulation of genes associated with TLR activation, DNA signaling, proinflammatory cytokines, chemokines, type 1 and 2 IFN response signatures, lymphocyte trafficking, MHC class 1 antigen presentation, B and T cell activation at 7 and 28 d PI in CON-fed mice than those fed DHA. Ingenuity Pathway Analysis (IPA) further demonstrated that DHA supplementation quelled cSiO<sub>2</sub>-induced responses top upstream regulators of proinflammatory and IFN-regulated gene networks to observed in CON-fed mice. Altogether, this short-term model illustrated that DHA suppression of aberrant acute cSiO<sub>2</sub>-induced inflammation is linked to altered regulation of autoimmune-related gene expression in lupus-prone mice.</p>
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>
DHA (Docosahexaenoic Acid), an Omega 3 Fatty Acid, in Slowing the Progression of Alzheimer's Disease
ClinicalTrials.gov study NCT00440050. IPD Sharing: Not stated. Countries: 1. Publications: 8.
Growth and Adiposity in Newborns: The Influence of Prenatal Docosahexaenoic Acid (DHA) Supplementation
ClinicalTrials.gov study NCT03310983. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Bridging the Docosahexaenoic Acid (DHA) Gap: The Effects of Omega-3 Fatty Acid Supplementation in Premature Infants
ClinicalTrials.gov study NCT01908907. IPD Sharing: NO. Countries: 1. Publications: 2.
Effects of Docosahexaenoic Acid (DHA) on Fetal Cardiac Outcomes
ClinicalTrials.gov study NCT01007110. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Data from: Dietary docosahexaenoic acid supplementation inhibits acute pulmonary transcriptional and autoantibody responses to a single crystalline silica exposure in lupus-prone mice
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Data from: Crystalline silica-induced proinflammatory eicosanoid storm in novel alveolar macrophage model quelled by docosahexaenoic acid
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Fig 5 in Docosahexaenoic Acid (DHA) Reduces LPS-Induced Inflammatory Response Via ATF3 Transcription Factor and Stimulates Src/Syk Signaling-Dependent Phagocytosis in Microglia
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Fig 3 in Docosahexaenoic Acid (DHA) Reduces LPSInduced Inflammatory Response Via ATF3 Transcription Factor and Stimulates Src/ Syk Signaling-Dependent Phagocytosis in Microglia
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Fig 4 in Docosahexaenoic Acid (DHA) Reduces LPS-Induced Inflammatory Response Via ATF3 Transcription Factor and Stimulates Src/Syk Signaling-Dependent Phagocytosis in Microglia
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Docosahexaenoic Acid (DHA) for Women With Breast Cancer in the Neoadjuvant Setting
ClinicalTrials.gov study NCT03831178. IPD Sharing: YES. Countries: 1. Publications: 2.
Effects of Docosahexaenoic Acid (DHA) on Children With Nonalcoholic Fatty Liver Disease (NAFLD)
ClinicalTrials.gov study NCT00885313. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Suppression of Postprandial Monocyte Activation by Blueberries or Docosahexaenoic Acid in Humans
ClinicalTrials.gov study NCT02472171. IPD Sharing: NO. Countries: 1. Publications: 1.
The DHA (Docosahexaenoic Acid) Oxford Learning and Behaviour (DOLAB) Study
ClinicalTrials.gov study NCT01066182. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Docosahexaenoic Acid (DHA) Supplementation in Amblyopia
ClinicalTrials.gov study NCT03402789. IPD Sharing: NO. Countries: 1. Publications: 5.
Docosahexaenoic Acid (DHA) Supplementation During Pregnancy Reduces the Risk of Preterm Birth in Threatened Preterm Labor
ClinicalTrials.gov study NCT06302023. IPD Sharing: YES. Countries: 1. Publications: 1.
The Effect of Supplemental Docosahexaenoic Acid (DHA) on Neurocognitive Outcomes in Teen and Adult Women With Phenylketonuria(PKU)
ClinicalTrials.gov study NCT00892554. IPD Sharing: Not stated. Countries: 1. Publications: 1.
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