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The Human Milk Oligosaccharide 3'Sialyllactose Promotes Selective Modulation of Inflammation and Reduces Atherosclerosis Development in Mice

ABSTRACT: The Human Milk Oligosaccharide 3'Sialyllactose Promotes Selective Modulation of Inflammation and Reduces Atherosclerosis Development in Mice

PROVIDER: PRJNA713785 | ENA |

REPOSITORIES: ENA

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The Human Milk Oligosaccharide 3'Sialyllactose Promotes Selective Modulation of Inflammation and Reduces Atherosclerosis Development in Mice

Project description:Macrophages contribute to the induction and resolution of inflammation and play a central role in the chronic low-grade inflammation in cardiovascular diseases caused by atherosclerosis. Human milk oligosaccharides (HMOs) are complex unconjugated glycans unique to human milk that benefit infant health and act as innate immune modulators. Here, we identify the HMO 3’sialyllactose (3’SL) as a natural inhibitor of TLR4-induced low-grade inflammation in macrophages and endothelium. Transcriptome analysis in macrophages revealed that 3’SL attenuates a selected set of inflammatory gene expression and promotes activity of genomic regions occupied by LXR and SREBP. These acute anti-inflammatory effects of 3’SL were associated with reduced histone H3K27 acetylation at a subset of LPS-inducible enhancers distinguished by preferential enrichment for NFKB, ATF3, IRF2, BCL6, and other transcription factor recognition motifs. In a murine atherosclerosis model, both subcutaneous and oral administration of 3’SL significantly reduced atherosclerosis development and the associated inflammation. This study provides evidence that 3’SL attenuates inflammation by a transcriptional mechanism to reduce atherosclerosis development in the context of cardiovascular disease.

2024-03-04 | GSE168730 | GEO

The Human Milk Oligosaccharide 3’Sialyllactose Promotes Inflammation Resolution and Reduces Atherosclerosis Development in Mice

Project description:The Human Milk Oligosaccharide 3’Sialyllactose Promotes Inflammation Resolution and Reduces Atherosclerosis Development in Mice

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The Human Milk Oligosaccharide 3’Sialyllactose Promotes Inflammation Resolution and Reduces Atherosclerosis Development in Mice

Project description:The Human Milk Oligosaccharide 3’Sialyllactose Promotes Inflammation Resolution and Reduces Atherosclerosis Development in Mice

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The Human Milk Oligosaccharide 3’Sialyllactose Promotes Inflammation Resolution and Reduces Atherosclerosis Development in Mice

Project description:Macrophages contribute to the induction and resolution of inflammation and play a central role in the chronic low-grade inflammation in cardiovascular diseases caused by atherosclerosis. Human milk oligosaccharides (HMOs) are complex unconjugated glycans unique to human milk that benefit infant health and act as innate immune modulators. Here, we identify the HMO 3’sialyllactose (3’SL) as a natural inhibitor of TLR4-induced low-grade inflammation in macrophages and endothelium. Transcriptome analysis in macrophages revealed that 3’SL attenuates a selected set of inflammatory gene expression and promotes activity of LXR and SREBP. These acute anti-inflammatory effects of 3’SL were associated with reduced histone H3K27 acetylation at a subset of LPS-inducible enhancers distinguished by preferential enrichment for CTCF, IRF2, BCL6, and other transcription factor recognition motifs. In a murine atherosclerosis model, both subcutaneous and oral administration of 3’SL significantly reduced atherosclerosis development and the associated inflammation. This study provides evidence that 3’SL attenuates inflammation by a transcriptional mechanism to reduce atherosclerosis development in the context of cardiovascular disease.

2024-10-20 | GSE186412 | GEO

The Human Milk Oligosaccharide 3’Sialyllactose Promotes Inflammation Resolution and Reduces Atherosclerosis Development in Mice

Project description:Macrophages contribute to the induction and resolution of inflammation and play a central role in the chronic low-grade inflammation in cardiovascular diseases caused by atherosclerosis. Human milk oligosaccharides (HMOs) are complex unconjugated glycans unique to human milk that benefit infant health and act as innate immune modulators. Here we identify the HMO 3’sialyllactose (3’SL) as a natural inhibitor of TLR4-induced low-grade inflammation in macrophages and endothelium. Transcriptome analysis in macrophages revealed that 3’SL attenuates a selected set of inflammatory gene expression and promotes activity of LXR and SREBP. Surprisingly, the acute anti-inflammatory effects of 3’SL were associated with reduced histone H3K27 acetylation at a subset of LPS-inducible enhancers distinguished by preferential enrichment for CTCF, IRF2, BCL6 and other transcription factor recognition motifs. In a murine atherosclerosis model, the subcutaneous administration of 3’SL significantly reduced atherosclerosis development and macrophage content in atherosclerotic lesions. This study provides evidence that 3’SL attenuates inflammation by a transcriptional mechanism to reduce atherosclerosis development in the context of cardiovascular disease.

2024-09-01 | GSE167999 | GEO

Mus musculus breed:C57Bl/LDLR-/-

Project description:Human Milk Oligosaccharide 3 Sialyllactose Promotes Inflammation Resolution and Reduces Atherosclerosis Development in Mice

| PRJNA996113 | ENA

Human Milk Oligosaccharide Interactions in Mouse Macrophage

Project description:Chemoproteomic profiling of Human Milk Oligosaccharide Interactions in Mouse Macrophages

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Chitin oligosaccharide induction

Project description:Strain N16961 grown in M9 + 0.5 % lactate to OD 0.2. Culture was split and one part added 0.6 mM of indicated chitin oligosaccharide. Samples was isolated after 30 and 60 min. cDNA was prepared from 2 ug RNA and labeled with Cy3 (no induction) and Cy5 (induction with chitin oligosaccharide). Samples from at least two independent experiments and a total of four hybridizations for each chitin oligosaccharide and time. A growth condition experiment design type is where some part of the growth condition is changed for the purposes of the experiment, examples of growth conditions changed are media, temperature, humidity, light, nutrients. Keywords: growth_condition_design

2005-08-11 | GSE3101 | GEO

Chitin oligosaccharide induction

2005-08-11 | E-GEOD-3101 | biostudies-arrayexpress

TRAF-STOPping atherosclerosis: targeting of CD40-induced TRAF6 signaling in macrophages reduces (established) atherosclerosis

Project description:Inhibition of the costimulatory CD40-CD40L receptor/ligand dyad drastically reduces atherosclerosis. However, its long-term blockage can result in immune suppression. We recently identified small molecule inhibitors that block the interaction between CD40 and TNF Receptor Associated Factor (TRAF) 6 (TRAF-STOPs), while leaving CD40-TRAF2/3/5 interactions intact, thereby preserving CD40-mediated immunity. Here we further characterized the working mechanisms of TRAF-STOPs 6877002 and 6860766 in atherogenesis. Transcriptional profiling in CD40-activated macrophages showed that TRAF-STOP 6877002 had profound effects on the clusters ‘immune responses’ and ‘cell cycle progression’, whereas TRAF-STOP 6860766 only affected ‘immune responses’.

2018-01-15 | GSE90835 | GEO

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