scholarly journals Human milk oligosaccharides prevent Necrotizing Enterocolitis in neonatal rats

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Lars Bode ◽  
Kerstin Goth ◽  
Yigit Guner ◽  
Caroline Nissan ◽  
Monica Zherebtsov ◽  
...  
Keyword(s):  
Human Milk ◽  
Necrotizing Enterocolitis ◽  
Neonatal Rats ◽  
Human Milk Oligosaccharides ◽  
Milk Oligosaccharides

scholarly journals The Role of Human Milk Oligosaccharides and Probiotics on the Neonatal Microbiome and Risk of Necrotizing Enterocolitis: A Narrative Review

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3052
Author(s):  
Lila S. Nolan ◽  
Jamie M. Rimer ◽  
Misty Good
Keyword(s):  
Human Milk ◽  
Preterm Infants ◽  
Necrotizing Enterocolitis ◽  
Mode Of Delivery ◽  
Intestinal Barrier ◽  
Vulnerable Population ◽  
Human Milk Oligosaccharides ◽  
Milk Oligosaccharides ◽  
Intestinal Homeostasis

Preterm infants are a vulnerable population at risk of intestinal dysbiosis. The newborn microbiome is dominated by Bifidobacterium species, though abnormal microbial colonization can occur by exogenous factors such as mode of delivery, formula feeding, and exposure to antibiotics. Therefore, preterm infants are predisposed to sepsis and necrotizing enterocolitis (NEC), a fatal gastrointestinal disorder, due to an impaired intestinal barrier, immature immunity, and a dysbiotic gut microbiome. Properties of human milk serve as protection in the prevention of NEC. Human milk oligosaccharides (HMOs) and the microbiome of breast milk are immunomodulatory components that provide intestinal homeostasis through regulation of the microbiome and protection of the intestinal barrier. Enteral probiotic supplements have been trialed to evaluate their impact on establishing intestinal homeostasis. Here, we review the protective role of HMOs, probiotics, and synbiotic combinations in protecting a vulnerable population from the pathogenic features associated with necrotizing enterocolitis.

scholarly journals A47 SYNTHETIC HUMAN MILK OLIGOSACCHARIDES PREVENT EXPERIMENTAL NECROTIZING ENTEROCOLITIS VIA DIVERGENT TRANSCRIPTOMIC RESPONSES.

2021 ◽  
Vol 4 (Supplement_1) ◽  
pp. 272-274
Author(s):  
R Y Wu ◽  
B Li ◽  
R Horne ◽  
A Ghamel ◽  
S Robinson ◽  
...  
Keyword(s):  
Immune Responses ◽  
Human Milk ◽  
Necrotizing Enterocolitis ◽  
Mucosal Injury ◽  
Intestinal Cell ◽  
Human Milk Oligosaccharides ◽  
Milk Oligosaccharides ◽  
In Vivo Models

Abstract Background Breastmilk reduces the risk of necrotizing enterocolitis (NEC) in preterm infants, but the bioactive components mediating this effect are not well understood. Human milk oligosaccharides (HMOs) reduce NEC both in humans and in relevant animal models. However, it is unclear if there are functional differences between individual oligosaccharides. Aims The objective of this study was to compare the intestinal transcriptome responses of individual HMOs using complementary in vitro and in vivo models of NEC. Methods RNA sequencing was performed on Caco-2Bbe1 gut epithelial cells after exposure to commercially-purified 2’-fucosyllactose (2’FL), 3-fucosyllactose, 6’-siallyllactose, lacto-N-tetraose (LNT) or lacto-N-neotetraose for 24hr at 37°C for 24 h (n=3). Signaling pathways were analyzed in murine- and human-derived NEC enteroids by qPCR. To validate these findings, five-day-old mouse pups were orally gavaged formula with or without individual HMOs, followed by NEC induction with hypoxia (5% O2, 95% N2) and lipopolysaccharide (4 mg/kg/day). Coded ileal sections (n=6–7/group) were analyzed for mucosal injury by histology, immune fluorescence, immunohistochemistry, and gene expression via qPCR. Results The HMO transcriptome clustered into divergent functional categories including metabolic process, protein processing and responses to external stimuli. Each synthetic HMO induced a unique transcriptome and exhibited varying effects on the intestinal epithelial functions and biological pathways. This was confirmed in the murine model of NEC, as both LNT and 2FL mitigated NEC injury with comparable recovery of intestinal cell proliferation (Ki67) and expression of stem cells (Lgr5+). Both qPCR and immunofluorescence staining showed differences between 2FL- and LNT-fed pups in host inflammatory and immune responses. Conclusions This study demonstrates that synthetic HMOs ameliorate intestinal injury in experimental NEC. However, the mechanisms by which individual oligosaccharides act on the intestine differ, suggesting that single synthetic HMOs may not fully recapitulate the benefits of pooled HMOs. Future studies will further delineate structure-function relationships of synthetic HMOs on host intestinal innate and adaptive immune responses. Funding Agencies CIHRFerring Canada Medical Student Research grant

scholarly journals Human milk oligosaccharides are differentially metabolised in neonatal rats

2013 ◽  
Vol 110 (4) ◽  
pp. 640-650 ◽  
Author(s):  
Evelyn Jantscher-Krenn ◽  
Carolin Marx ◽  
Lars Bode
Keyword(s):  
Small Intestine ◽  
Human Milk ◽  
Neonatal Rats ◽  
Human Milk Oligosaccharides ◽  
Milk Oligosaccharides ◽  
Target Organs ◽  
Mother's Milk ◽  
Mother’S Milk ◽  
Breast Fed

Human milk oligosaccharides (HMO) are complex glycans that are highly abundant in human milk, but not in infant formula. Accumulating data, mostly from in vitro and animal studies, indicate that HMO benefit the breast-fed infant in multiple ways and in different target organs. In vitro incubation studies suggest that HMO can resist the low pH in the infant's stomach and enzymatic degradation in the small intestine and reach the colon in the same composition as in the mother's milk. The oligosaccharide composition in faeces of breast-fed infants is, however, very different from that in the mother's milk, raising questions on when, where and how HMO are metabolised between ingestion and excretion. To answer some of these questions, we established a pulse-chase model in neonatal rats and analysed HMO profiles to track their composition over time in five consecutive equal-length intestinal segments as well as in serum and urine. The relative abundance of individual HMO changed significantly within the first 2 h after feeding and already in the segments of the small intestine prior to reaching the colon. Only 3′-sialyllactose, the major oligosaccharide in rat milk, and hardly any other HMO appeared in the serum and the urine of HMO-fed rats, indicating a selective absorption of rat milk-specific oligosaccharides. The present results challenge the paradigm that HMO reach the colon and other target organs in the same composition as originally secreted with the mother's milk. The present results also raise questions on whether rats and other animals represent suitable models to study the effects of HMO.

scholarly journals Human Milk Oligosaccharides to Prevent Gut Dysfunction and Necrotizing Enterocolitis in Preterm Neonates

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1461 ◽  
Author(s):  
Stine Bering
Keyword(s):  
Preterm Birth ◽  
Human Milk ◽  
Preterm Infants ◽  
Necrotizing Enterocolitis ◽  
Bacterial Colonization ◽  
Health Benefits ◽  
Preterm Neonates ◽  
Human Milk Oligosaccharides ◽  
High Concentration ◽  
Milk Oligosaccharides

This review focuses on the evidence for health benefits of human milk oligosaccharides (HMOs) for preterm infants to stimulate gut adaptation and reduce the incidence of necrotizing enterocolitis (NEC) in early life. The health benefits of breastfeeding are partly explained by the abundant HMOs that serve as prebiotics and immunomodulators. Gut immaturity in preterm infants leads to difficulties in tolerating enteral feeding and bacterial colonization and a high sensitivity to NEC, particularly when breast milk is insufficient. Due to the immaturity of the preterm infants, their response to HMOs could be different from that in term infants. The concentration of HMOs in human milk is highly variable and there is no evidence to support a specifically adapted high concentration in preterm milk. Further, the gut microbiota is not only different but also highly variable after preterm birth. Studies in pigs as models for preterm infants indicate that HMO supplementation to formula does not mature the gut or prevent NEC during the first weeks after preterm birth and the effects may depend on a certain stage of gut maturity. Supplemented HMOs may become more important for gut protection in the preterm infants when the gut has reached a more mature phase.

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