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Updated: Mar 27, 2026

A Macrophage Reporter Cell Assay to Examine Toll-Like Receptor-Mediated NF-kB/AP-1 Signaling on Adsorbed Protein Layers on Polymeric Surfaces
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Human Milk Components Modulate Toll-Like Receptor-Mediated Inflammation.

YingYing He1, Nathan T Lawlor1, David S Newburg2

  • 1Program in Glycobiology, Department of Biology, Boston College, Chestnut Hill, MA.

Advances in Nutrition (Bethesda, Md.)
|January 17, 2016
PubMed
Summary

Human milk contains bioactive components that regulate Toll-like receptor (TLR) signaling, crucial for innate immunity. These components offer potential treatments for neonatal inflammatory diseases by modulating TLR pathways.

Keywords:
glycanshuman milkimmune functioninflammationtoll like receptors

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Area of Science:

  • Immunology
  • Neonatal Medicine
  • Gastroenterology

Background:

  • Toll-like receptor (TLR) signaling is fundamental to innate immunity.
  • Abnormal TLR expression is implicated in neonatal inflammatory diseases.
  • Human milk contains various bioactive components that modulate TLRs.

Purpose of the Study:

  • To investigate the role of human milk components in modulating TLR signaling pathways.
  • To explore the potential of these components in managing neonatal inflammatory conditions.

Main Methods:

  • Analysis of bioactive components in human milk.
  • Assessment of their impact on TLR expression and signaling pathways (TLR2, TLR3, TLR4, TLR7).

Main Results:

  • Specific milk components like sialyl(α2,3)lactose and lacto-N-fucopentaose III can increase TLR signaling.
  • Other components, including soluble TLR2 (sTLR2), soluble CD14 (sCD14), lactadherin, lactoferrin, 2'-fucosyllactose, 3'-galactosyllactose, and β-defensin 2, inhibit TLR signaling.
  • Human milk consumption is associated with reduced risk of sepsis and necrotizing enterocolitis in neonates.

Conclusions:

  • Human milk possesses potent anti-inflammatory properties mediated by TLR-modulating components.
  • These milk-derived compounds show promise for oral prophylactic and therapeutic use in TLR-mediated gastrointestinal inflammatory disorders.