Chelsea D. Painter
Research Subjects
Research Interests
Chelsea D. Painter has a total of 32 co-authors. Here are the top co-authors by number of shared publications:
- Adam P. Cribbs
Botnar Research Centre, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, National Institute of Health Research Oxford Biomedical Research Unit (BRU), University of Oxford, Oxford, UK
1 shared publication - Alexandra Hammond
Department of Pediatrics at UCSD, La Jolla, California, USA
1 shared publication - Annette R. Atkins
Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California, USA
1 shared publication - Anthony Quach
Department of Medicine, UCSD, La Jolla, California, USA
1 shared publication - Ariane R. Pessentheiner
Department of Medicine, UCSD, La Jolla, California, USA
1 shared publication - Austin Wan-Tien Chiang
Department of Pediatrics, University of California, San Diego, La Jolla, CA 92093, USA,; Immunology Center of Georgia, Augusta University, Augusta, GA, United States
1 shared publication
Latest Publications
- Open Access
- 8 November 2024
- Published by American Society for Clinical Investigation in JCI Insight
- Vol. 9 (21)
The human milk oligosaccharide 3′sialyllactose reduces low-grade inflammation and atherosclerosis development in mice
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.
- 8 November 2024
- Published by American Society for Clinical Investigation in JCI Insight
- Vol. 9 (21)
Open AccessThe human milk oligosaccharide 3′sialyllactose reduces low-grade inflammation and atherosclerosis development in mice
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.