scholarly journals Protective Effects of Human Milk Oligosaccharides on Intestinal Epithelial Function Assessed in Enteroid‐Derived Monolayers

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Alice Drobny ◽  
Stella Rita Ibeawuchi ◽  
Soumita Das ◽  
Lars Bode ◽  
Kim Elaine Barrett
2021 ◽  
Author(s):  
Chunli Kong ◽  
Martin Beukema ◽  
Min Wang ◽  
Bart J. de Haan ◽  
Paul de Vos

Human milk oligosaccharides 2′-FL and pectins inhibited pathogen adhesion through modulating glycosylation and inflammatory genes in intestinal epithelial cells.


2020 ◽  
Vol 150 (8) ◽  
pp. 2077-2088 ◽  
Author(s):  
Chunli Kong ◽  
Lianghui Cheng ◽  
Guido Krenning ◽  
Jolien Fledderus ◽  
Bart J de Haan ◽  
...  

ABSTRACT Background The intestinal epithelial cells, food molecules, and gut microbiota are continuously exposed to intestinal peristaltic shear force. Shear force may impact the crosstalk of human milk oligosaccharides (hMOs) with commensal bacteria and intestinal epithelial cells. Objectives We investigated how hMOs combined with intestinal peristaltic shear force impact intestinal epithelial cells and crosstalk with a commensal bacterium. Methods We applied the Ibidi system to mimic intestinal peristaltic shear force. Caco-2 cells were exposed to a shear force (5 dynes/cm2) for 3 d, and then stimulated with the hMOs, 2′-fucosyllactose (2′-FL), 3-FL, and lacto-N-triose II (LNT2). In separate experiments, Lactobacillus plantarumWCFS1 adhesion to Caco-2 cells was studied with the same hMOs and shear force. Effects were tested on gene expression of glycocalyx-related molecules (glypican 1 [GPC1], hyaluronan synthase 1 [HAS1], HAS2, HAS3, exostosin glycosyltransferase 1 [EXT1], EXT2), defensin β-1 (DEFB1), and tight junction (tight junction protein 1 [TJP1], claudin 3 [CLDN3]) in Caco-2 cells. Protein expression of tight junctions was also quantified. Results Shear force dramatically decreased gene expression of the main enzymes for making glycosaminoglycan side chains (HAS3 by 43.3% and EXT1 by 68.7%) (P <0.01), but did not affect GPC1 which is the gene responsible for the synthesis of glypican 1 which is a major protein backbone of glycocalyx. Expression of DEFB1, TJP1, and CLDN3 genes was decreased 60.0–94.9% by shear force (P <0.001). The presence of L. plantarumWCFS1 increased GPC1, HAS2, HAS3, and ZO-1 expression by 1.78- to 3.34-fold (P <0.05). Under shear force, all hMOs significantly stimulated DEFB1 and ZO-1, whereas only 3-FL and LNT2 enhanced L. plantarumWCFS1 adhesion by 1.85- to 1.90-fold (P <0.01). Conclusions 3-FL and LNT2 support the crosstalk between the commensal bacterium L. plantarumWCFS1 and Caco-2 intestinal epithelial cells, and shear force can increase the modulating effects of hMOs.


2019 ◽  
Vol 63 (17) ◽  
pp. 1900303 ◽  
Author(s):  
Chunli Kong ◽  
Marlies Elderman ◽  
Lianghui Cheng ◽  
Bart J. Haan ◽  
Arjen Nauta ◽  
...  

2015 ◽  
Vol 145 (9) ◽  
pp. 1992-1998 ◽  
Author(s):  
Sara Gonia ◽  
Michele Tuepker ◽  
Timothy Heisel ◽  
Chloe Autran ◽  
Lars Bode ◽  
...  

2021 ◽  
Vol 8 ◽  
Author(s):  
Safiyyah Abbas ◽  
Amy K. Keir ◽  
Maria Makrides ◽  
Laura D. Klein ◽  
Luke E. Grzeskowiak ◽  
...  

Necrotising enterocolitis (NEC) is a devastating disease affecting preterm infants, with little improvement in mortality rates and treatment strategies in the last 30 years. Human milk oligosaccharides (HMOs) are emerging as a potential preventive therapy, with multiple protective functions postulated. Our aim is to summarise the evidence concerning the role of HMOs in NEC development and emerging strategies to tailor the delivery of HMOs to preterm infants. Most research efforts to date have focused on supplementing preterm infants with simple oligosaccharides, which are structurally different to HMOs and derived mainly from plants. Clinical trials demonstrate limited benefits for NEC prevention arising from the use of these supplements. Alternative strategies under investigation include optimising HMOs for infants receiving donor human milk, concentrating oligosaccharides from donor human milk and from animal milks, as well as more sophisticated synthetic oligosaccharide production strategies. Critically, high quality evidence to support implementation of any of these approaches in the neonatal unit is lacking. Whether it is a specific HMO alone or a combination of HMOs that exert protective effects remains to be elucidated. Further challenges include how best to manufacture and administer oligosaccharides whilst retaining bioactivity and safety, including evaluation of the long-term effects of altering the balance of HMOs and gut microbiota in preterm infants. While several human clinical trials are underway, further research is needed to understand whether a tailored approach to oligosaccharide supplementation is beneficial for preterm infants.


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