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Lactodifucotetraose, a human milk oligosaccharide, attenuates platelet function and inflammatory cytokine release
David S Newburg1, Ayse C Tanritanir2, Subrata Chakrabarti2
1Higgins Hall - Biology, Boston College, 140 Commonwealth Avenue, Chestnut Hill, MA, 02467, USA. newburgd@bc.edu.
Insights
Human milk oligosaccharides, particularly lactodifucotetraose (LDFT), reduce inflammatory responses in infant platelets. This suggests LDFT may offer therapeutic benefits for inflammatory conditions in both infants and adults.
Area of Science:
- Immunology
- Neonatal Physiology
- Biochemistry
Background:
- Human milk possesses anti-inflammatory properties, benefiting breastfed infants who exhibit lower inflammatory disease rates.
- Neonatal platelets are less responsive to agonists compared to adult platelets.
- Breastfed infants absorb intact human milk oligosaccharides into circulation.
Purpose of the Study:
- To investigate if human milk oligosaccharides can modulate infant platelet function.
- To determine if oligosaccharides can reduce pro-inflammatory protein secretion from platelets.
- To identify the specific active oligosaccharide component responsible for these effects.
Main Methods:
- Platelets from human blood were isolated and exposed to thrombin, ADP, and collagen.
- The effects of a natural human milk oligosaccharide mixture and individual purified oligosaccharides were tested.
- Inhibition of platelet adhesion, aggregation, and inflammatory protein release (RANTES, sCD40L) was measured.
Main Results:
- Human milk and its oligosaccharide mixture inhibited inflammatory protein release from platelets.
- Lactodifucotetraose (LDFT) significantly inhibited thrombin-induced RANTES and sCD40L release.
- LDFT also reduced platelet adhesion to collagen and aggregation induced by ADP or collagen.
Conclusions:
- Lactodifucotetraose (LDFT) demonstrates potent anti-inflammatory effects on platelets.
- LDFT may play a role in modulating hemostasis and suppressing inflammation in breastfed infants.
- Further research into LDFT as a therapeutic agent for inflammatory conditions is warranted.
Abstract:
Human milk strongly quenches inflammatory processes in vitro, and breastfed infants have lower incidence of inflammatory diseases than those fed artificially. Platelets from neonates, in contrast to those from adults, are less responsive to platelet agonists such as collagen, thrombin, ADP, and epinephrine. Breastfed infants absorb oligosaccharides intact from the human milk in their gut to the circulation. This study was to determine whether these oligosaccharides can attenuate platelet function and platelet secretion of pro-inflammatory proteins, and to identify the active component. The natural mixture of oligosaccharides from human milk and pure individual human milk oligosaccharides were tested for their ability to modulate responses of platelets isolated from human blood following exposure to thrombin, ADP, and collagen. Human milk and the natural mixture of human milk oligosaccharides inhibited platelet release of inflammatory proteins. Of the purified human milk oligosaccharides tested, only lactodifucotetraose (LDFT) significantly inhibited thrombin induced release of the pro-inflammatory proteins RANTES and sCD40L. LDFT also inhibited platelet adhesion to a collagen-coated surface, as well as platelet aggregation induced by ADP or collagen. These data indicate that LDFT may help modulate hemostasis by suppressing platelet-induced inflammatory processes in breastfed infants. This activity suggests further study of LDFT for its potential as a therapeutic agent in infants and adults.
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