ArticleJCI insight2024
The human milk oligosaccharide 3'sialyllactose reduces low-grade inflammation and atherosclerosis development in mice.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Short-term modulation of human milk oligosaccharides in plasma and milk by glucose and insulin: insights into postpartum metabolic regulation.Diabetologia · 2026Article
- Human Milk Oligosaccharides: Shaping the Anti-Infective Status in Infancy.Microorganisms · 2026Review
- Development and application of synthetic biology tools for improved production of human breast milk components.Synthetic and systems biotechnology · 2025Review
- Systemic Availability of Human Milk Oligosaccharides in Infants and Adults: A Narrative Review.Advances in nutrition (Bethesda, Md.) · 2025Review
- Dietary 3'-sialyllactose reduces sensitization and type 2 inflammation in a house dust mite induced acute allergic asthma model.Frontiers in allergy · 2025Article
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Authors and funding
33 authors.
Funding
Abstract
Macrophages contribute to the induction and resolution of inflammation and play a central role in 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 mRNA levels of a selected set of inflammatory genes and promotes the activity of liver X receptor (LXR) and sterol regulatory element binding protein-1 (SREBP1). These acute antiinflammatory effects of 3'SL were associated with reduced histone H3K27 acetylation at a subset of LPS-inducible enhancers distinguished by preferential enrichment for CCCTC-binding factor (CTCF), IFN regulatory factor 2 (IRF2), B cell lymphoma 6 (BCL6), and other transcription factor recognition motifs. In a murine atherosclerosis model, both s.c. 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.
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Registered trials
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