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Published on: May 21, 2018
Whey protein hydrolysates decrease IL-8 secretion in lipopolysaccharide (LPS)-stimulated respiratory epithelial cells
Michèle M Iskandar1, Nurlan Dauletbaev, Stan Kubow
1School of Dietetics and Human Nutrition, Macdonald Campus of McGill University, Sainte Anne de Bellevue, QC, Canada H9X 3V9.
Pressurised whey peptides show enhanced anti-inflammatory effects by reducing lipopolysaccharide (LPS) binding to Toll-like receptor 4 (TLR4) and boosting antioxidant capacity, benefiting cystic fibrosis (CF) respiratory cells.
Area of Science:
- Biochemistry
- Immunology
- Cell Biology
Background:
- Whey proteins (WP) possess anti-inflammatory and antioxidant properties.
- Hyperbaric pressurisation enhances WP digestibility and peptide release.
- Dietary pressurised whey supplementation improves nutritional status and systemic inflammation in cystic fibrosis (CF) patients.
Purpose of the Study:
- To investigate the anti-inflammatory effects of peptides from pressurised whey (pWP) hydrolysates on CF respiratory epithelial cells.
- To determine if pWP peptides can attenuate inflammatory responses stimulated by lipopolysaccharide (LPS).
Main Methods:
- In vitro generation of hydrolysates from pressurised WP (pWP) and native WP (nWP).
- Testing of hydrolysates for anti-inflammatory properties by measuring IL-8 production in CF and non-CF respiratory epithelial cell lines.
- Assessment of LPS binding to Toll-like receptor 4 (TLR4) and extracellular antioxidant capacity.
Main Results:
- pWP hydrolysate demonstrated a greater suppression of LPS-stimulated IL-8 production compared to nWP hydrolysate in both cell lines.
- Neither hydrolysate affected IL-8 production induced by TNF-α or IL-1β, suggesting a specific effect on the TLR4 pathway.
- Both hydrolysates reduced LPS binding to TLR4, with pWP showing a more potent increase in extracellular antioxidant capacity.
Conclusions:
- Pressurisation enhances the anti-inflammatory properties of whey peptides.
- The suppression of IL-8 production by pWP peptides, via reduced LPS binding to TLR4 and enhanced antioxidant capacity, may contribute to clinical benefits in CF patients.
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