Lipid Metabolism in Inflammation and Immune Function

Andersen, Catherine J.

doi:10.3390/nu14071414

Cited by 44 publications

(18 citation statements)

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“…Inflammation and lipid signaling are intertwined modulators of homeostasis and immunity. 35 As reported, the crosstalk between metabolism, microbes, and immunity and their interplay is associated with the pathogenesis of NAFLD. 36 Lipid deposition in the liver caused by lipid metabolism disorder is deemed as the direct cause of NAFLD.…”

Section: Discussionmentioning

confidence: 91%

Asprosin contributes to nonalcoholic fatty liver disease through regulating lipid accumulation and inflammatory response via AMPK signaling

Zhang,

Lu,

Jiang

et al. 2023

Immunity Inflam & Disease

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BackgroundNonalcoholic fatty liver disease (NAFLD) is a primary contributor to liver‐related morbidity and mortality. Asprosin has been reported to be implicated in NAFLD.AimsThis work is to illuminate the effects of Asprosin on NAFLD and the possible downstream mechanism.Materials & MethodsThe weight of NAFLD mice induced by a high‐fat diet was detected. Quantitative reverse‐transcription polymerase chain reaction (RT‐qPCR) examined serum Asprosin expression. RT‐qPCR and western blot analysis examined Asprosin expression in mice liver tissues. Intraperitoneal glucose tolerance test (IPGTT) and intraperitoneal insulin tolerance test (IPITT) were implemented. Biochemical kits tested liver enzyme levels in mice serum and liver tissues. Hematoxylin and eosin staining evaluated liver histology. Liver weight was also tested and oil red O staining estimated lipid accumulation. RT‐qPCR and western blot analysis analyzed the expression of gluconeogenesis‐, fatty acid biosynthesis‐, fatty acid oxidation‐, and inflammation‐associated factors. Besides, western blot analysis examined the expression of AMP‐activated protein kinase (AMPK)/p38 signaling‐associated factors. In palmitic acid (PA)‐treated mice hepatocytes, RT‐qPCR and western blot analysis examined Asprosin expression. Lipid accumulation, gluconeogenesis, fatty acid biosynthesis, fatty acid oxidation, and inflammation were appraised again.ResultsAsprosin was overexpressed in the serum and liver tissues of NAFLD mice and PA‐treated mice hepatocytes. Asprosin interference reduced mice body and liver weight, improved glucose tolerance and diminished liver injury in vivo. Asprosin knockdown alleviated lipid accumulation and inflammatory infiltration both in vitro and in vivo. Additionally, Asprosin absence activated AMPK/p38 signaling and AMPK inhibitor Compound C reversed the impacts of Asprosin on lipid accumulation and inflammatory response.ConclusionCollectively, Asprosin inhibition suppressed lipid accumulation and inflammation to obstruct NAFLD through AMPK/p38 signaling.

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Section: Discussionmentioning

confidence: 91%

Asprosin contributes to nonalcoholic fatty liver disease through regulating lipid accumulation and inflammatory response via AMPK signaling

Zhang,

Lu,

Jiang

et al. 2023

Immunity Inflam & Disease

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“…In addition, main fraction HDL-associated apolipoprotein A1 (HDA1) and subfraction HDL-4 apolipoprotein A1 (H4A1) were observed to be lower in the plasma of the burn injury group compared to non-burn controls. HDLassociated apolipoprotein A1 has been reported to play an anti-inflammatory role in diseased states, due to its ability to carry anti-inflammatory molecules, bioactive lipids and cholesterol 13,55 . Depleted HDL-4 plasma concentrations have also been associated with poor outcomes and mortality in patients with pulmonary arterial hypertension 56 as well as a significant lipoprotein marker of SARS-CoV-2 infections 34,57 .…”

Section: Resultsmentioning

confidence: 99%

“…Processed data from the lipid profiling of non-burn and burn cohorts were robust, with intermittently run quality QC pooled plasma samples demonstrating tight clustering on a PCA scores plot (Figure S1B). Alterations in plasma lipid profiles have previously been observed following severe burn injuries, and were reported to be a result of systemic inflammatory responses 13 . Our data indicated differences in lipidomic profiles between plasma samples collected from the non-burn controls and burn injury group at both admission and 6 weeks post-surgery (Figure 4).…”

Section: Non-severe Burn Injury Causes Changes In Plasma Lipidomic Pr...mentioning

confidence: 99%

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Non-severe burns induce a prolonged systemic metabolic phenotype indicative of a persistent inflammatory response post-injury

Ryan

Raby

Masuda

et al. 2023

Preprint

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To understand the metabolic consequences following non-severe burns, longitudinal plasma was collected from adults with non-severe burn injuries (n=35) within 48 hours of admission to hospital and at 6 weeks post-surgery, as well as non-burn controls (n=14). Samples were analysed by 1H nuclear magnetic resonance spectroscopy and liquid chromatography-tandem mass spectrometry to quantify 112 lipoprotein, supramolecular phospholipid composite (SPC), GlycB arising from the glycoprotein N-acetylneuraminidino groups and 852 lipid species across 20 chemical subclasses. Alterations in lipoprotein and lipid metabolism were evident in samples taken within 48 hours of admission and found to be sustained at the 6-week timepoint, with increases in GlycB signal (p-value < 0.0001) and the multivariate importance of the apolipoprotein B100/apolipoprotein A1 (ABA1) ratio, as well as decreases in anti-inflammatory phosphatidylcholines, phosphatidylglycerols, phosphatidylinositols and phosphatidylserines. Low circulating high density lipoproteins, and increases in pro-atherogenic low density lipoproteins and monoacylglyceride (20:4) (p-value < 0.0001) are potentially indicative of an increased risk of cardiovascular disease after non-severe burns which requires further investigation.

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“…WES technology showed that EGCG downregulated NF-κB, which shows a flavonoid intervention in regulating inflammatory action. More research is necessary to understand the roles of mTOR, NF-kB, and Akt signaling in mediating the lipid metabolic effects on aging and neuroinflammation [ 89 , 90 ]. Research mechanisms of Tau protein contributions to aggregation were previously discussed in our prior work [ 91 ], but their relationship to microglial inflammation [ 92 ] and signaling mechanisms has yet to be determined.…”

Section: Discussionmentioning

confidence: 99%

Molecular Mechanisms of the Anti-Inflammatory Effects of Epigallocatechin 3-Gallate (EGCG) in LPS-Activated BV-2 Microglia Cells

et al. 2023

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Chronic neuroinflammation is associated with many neurodegenerative diseases, such as Alzheimer’s. Microglia are the brain’s primary immune cells, and when activated, they release various proinflammatory cytokines. Several natural compounds with anti-inflammatory and antioxidant properties, such as epigallocatechin 3-gallate (EGCG), may provide a promising strategy for inflammation-related neurodegenerative diseases involving activated microglia cells. The objective of the current study was to examine the molecular targets underlying the anti-inflammatory effects of EGCG in activated microglia cells. BV-2 microglia cells were grown, stimulated, and treated with EGCG. Cytotoxicity and nitric oxide (NO) production were evaluated. Immunoassay, PCR array, and WES™ Technology were utilized to evaluate inflammatory, neuroprotective modulators as well as signaling pathways involved in the mechanistic action of neuroinflammation. Our findings showed that EGCG significantly inhibited proinflammatory mediator NO production in LPS-stimulated BV-2 microglia cells. In addition, ELISA analysis revealed that EGCG significantly decreases the release of proinflammatory cytokine IL-6 while it increases the release of TNF-α. PCR array analysis showed that EGCG downregulated MIF, CCL-2, and CSF2. It also upregulated IL-3, IL-11, and TNFS10. Furthermore, the analysis of inflammatory signaling pathways showed that EGCG significantly downregulated mRNA expression of mTOR, NF-κB2, STAT1, Akt3, CCL5, and SMAD3 while significantly upregulating the expression of mRNA of Ins2, Pld2, A20/TNFAIP3, and GAB1. Additionally, EGCG reduced the relative protein expression of NF-κB2, mTOR, and Akt3. These findings suggest that EGCG may be used for its anti-inflammatory effects to prevent neurodegenerative diseases.

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Lipid Metabolism in Inflammation and Immune Function

Abstract: Lipid metabolism plays an essential role in modulating inflammation within the context of acute and chronic diseases [...]

Cited by 44 publications

References 10 publications

Asprosin contributes to nonalcoholic fatty liver disease through regulating lipid accumulation and inflammatory response via AMPK signaling

Asprosin contributes to nonalcoholic fatty liver disease through regulating lipid accumulation and inflammatory response via AMPK signaling

Non-severe burns induce a prolonged systemic metabolic phenotype indicative of a persistent inflammatory response post-injury

Molecular Mechanisms of the Anti-Inflammatory Effects of Epigallocatechin 3-Gallate (EGCG) in LPS-Activated BV-2 Microglia Cells

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