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

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.

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3052
Author(s):  
Lila S. Nolan ◽  
Jamie M. Rimer ◽  
Misty Good

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.


2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Lars Bode ◽  
Kerstin Goth ◽  
Yigit Guner ◽  
Caroline Nissan ◽  
Monica Zherebtsov ◽  
...  

2020 ◽  
Author(s):  
Sylwia Jarzynka ◽  
Kamila Strom ◽  
Oliwia Makarewicz ◽  
Anna Minkiewicz-Zochniak ◽  
Anna Koryszewska-Baginska ◽  
...  

<p><strong>Background</strong>: Human milk oligosaccharides (HMOs) are the third most abundant component of breast milk, after fat and lactose, that promote infant health. Recent studies have shown that HMOs demonstrated antimicrobial and antibiofilm activity against different strains. Cystic fibrosis (CF), it is one of the major respiratory diseases, the clinical management and definitive treatment of CF biofilm-mediated chronic bacterial lung infection remains a challenge.</p> <p><strong>Objective</strong>: In this study, we examine HMOs antibiofilm activity against pathogens isolated from CF patients.</p> <p><strong>Methods and results</strong>: In current work, we investigated the antibiofilm activity of the saccharide fraction obtained from pooled human milk of 9 donors against strains of: <em>Acinetobacter baumannii</em>, <em>Pseudomonas aeruginosa</em>, <em>Enterobacteriaceae</em>, <em>Staphylococcus aureus</em> and <em>Burkholderia cenocepacia</em>, an intrinsically multi-resistant pathogen associated with high mortality in CF patients. We tested the ability of HMOs to inhibit biofilm formation and to eradicate matured biofilms. Live/dead staining of the biofilms and CLSM image acquisition were used.</p> <p>The pooled HMOs showed a biofilm eradicating effect on most tested pathogens. The HMOs effectively killed the bacteria at high concentration (20 mg/ml, corresponds to the concentration in human milk), but visible reduction of viable bacteria and biofilm mass was observed already at lower concentrations that varied between the species. The biofilm mass was also reduced in almost all pathogenic biofilms.</p> <p>The data presented in this paper supporting the importance and potential inhibitory effect of HMOs in biofilm formation. HMOs could potentially be used as novel therapeutics to treat or prevent infectious disease in patient with CF.</p>


2022 ◽  
Vol 9 ◽  
Author(s):  
Sarah Bajorek ◽  
Rebbeca M. Duar ◽  
Maxwell Corrigan ◽  
Christa Matrone ◽  
Kathryn A. Winn ◽  
...  

Not all infants carry specialized gut microbes, meaning they cannot digest human milk oligosaccharides and therefore do not receive complete benefits from human milk. B. infantis EVC001 is equipped to convert the full array of complex oligosaccharides into compounds usable by the infant, making it an ideal candidate to stabilize gut function and improve nutrition in preterm infants. A prospective, open-label study design was used to evaluate the tolerability of B. infantis EVC001 and its effects on the fecal microbiota in preterm infants in a Neonatal Intensive Care Unit. Thirty preterm infants <1,500 g and/or <33 weeks gestation at birth were divided into two matched groups, and control infants were enrolled and discharged prior to enrolling EVC001 infants to prevent cross-colonization of B. infantis: (1) fifteen control infants received no EVC001, and (2) fifteen infants received once-daily feedings of B. infantis EVC001 (8.0 x 109 CFU) in MCT oil. Clinical information regarding medications, growth, nutrition, gastrointestinal events, diagnoses, and procedures was collected throughout admission. Infant stool samples were collected at baseline, Study Days 14 and 28, and 34-, 36-, and 38-weeks of gestation. Taxonomic composition of the fecal microbiota, functional microbiota analysis, B. infantis, and human milk oligosaccharides (HMOs) in the stool were determined or quantified using 16S rRNA gene sequencing, metagenomic sequencing, qPCR, and mass spectrometry, respectively. No adverse events or tolerability issues related to EVC001 were reported. Control infants had no detectable levels of B. infantis. EVC001 infants achieved high levels of B. infantis (mean = 9.7 Log10 CFU/μg fecal DNA) by Study Day 14, correlating with less fecal HMOs (ρ = −0.83, P < 0.0001), indicating better HMO utilization in the gut. In this study, B. infantis EVC001 was shown to be safe, well-tolerated, and efficient in colonizing the preterm infant gut and able to increase the abundance of bifidobacteria capable of metabolizing HMOs, resulting in significantly improved utilization of human milk.Clinical Trial Registration:https://clinicaltrials.gov/ct2/show/NCT03939546, identifier: NCT03939546.


2019 ◽  
Author(s):  
Manuela-Raluca Pausan ◽  
Vassiliki Kolovetsiou-Kreiner ◽  
Gesa Lucia Richter ◽  
Tobias Madl ◽  
Elisabeth Giselbrecht ◽  
...  

AbstractBackgroundPreterm birth is one of the leading causes of neonatal mortality. The causes for spontaneous preterm birth (PTB) are multifactorial and remain often unknown. In this study, we tested the hypothesis that human milk oligosaccharides (HMOs) in blood and urine modulate the maternal urinary and vaginal microbiome and influence the risk for PTB. We analyzed the vaginal and urinary microbiome of a cross-sectional cohort of women with and without preterm labor and correlated our findings with measurements of metabolites and HMOs in urine and blood.ResultsWe identified several microbial signatures associated with short cervix, PTB and/or preterm contractions such asLactobacillus jensenii,L. gasseri,Ureaplasma sp. andGardnerella sp..Additionally, we observed associations between sialylated HMOs, in particular 3’-sialyllactose, with PTB, short cervix and increased inflammation and confirmed an influence of HMOs on the microbiome profile.ConclusionsIdentifying serum and urinary HMOs and several key microorganisms associated with PTB, our findings point at two distinct processes modulating the risk for PTB. One process seems to be driven by sterile inflammation, characterized by increased concentrations of sialylated HMOs in serum. Another process might be microbiome-mediated, potentially driven by secretor-active HMOs in urine. Our results support current efforts to improve diagnostics and therapeutic strategies.


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