Search Results (3)

Background/Objectives: After birth, mothers provide the best nutrition for the healthy growth and development of their infants and the developing gut microbiota through breastfeeding. When breastfeeding is not or insufficiently available, infant formula is the only safe alternative. The production of infant formula includes heat-processing, which may induce protein glycation. Protein glycation has been shown to reduce protein digestion and absorption. The reduction in protein digestion and absorption because of protein glycation has been speculated to also impact gut comfort parameters as well as overnight sleep. Methods: As this could be partially due to the effect on the bacteria that reside in the infant’s gastrointestinal tract, we investigated whether protein glycation in infant formula impacts the composition and activity of infant gut microbiota by performing an in vitro study using the CoMiniGut colon model and fecal inocula obtained from a healthy six-month-old term infant. Incubations were performed for 24 h using a predigested infant formula-supplemented medium with varying levels of glycation (6.5–44.5%). Results: Our data indicate that high protein glycation increases microbial diversity and the relative abundance of Clostridium neonatale from 6.4% of the inoculum to around 25.5% of 20.8% glycation. Interestingly, propionate levels were inversely correlated with protein glycation levels after 24 h of incubation, with the 44.5% blocked lysine sample giving rise to 60% lower propionate levels as compared to the 6.4% sample. Higher propionate levels have been linked with longer uninterrupted sleep overnight, which could be indicative of the underlying mechanism of reduced crying/fussy time during nights for infants fed with a formula containing lower amounts of glycated protein. Full article

Background: Necrotizing enterocolitis (NEC) is still one of the leading causes of neonatal death. The present study reports the data from a French case–control prospective multicenter study. Methods: A total of 146 preterm neonates (PNs) with or without NEC were included. Bacterial 16S rRNA gene sequencing was performed on stool samples (n = 103). Specific culture media were used to isolate Escherichia coli, Clostridium butyricum, and Clostridium neonatale, and strains were phenotypically characterized. Results: The gut microbiota of PNs was dominated by Firmicutes and Proteobacteria, and five enterotypes were identified. The microbiota composition was similar between NEC cases and PN controls. However, differences were observed in the relative abundance of Lactobacillus genus, which was significantly lower in the NEC group, whereas that of the Clostridium cluster III was significantly higher (p < 0.05). Within enterotypes, several phylotypes were significantly more abundant in NEC cases (p < 0.05). Regarding perinatal factors, a statistical association was found between the gut microbiota and cesarean delivery and antifungal therapy. In NEC cases and PN controls, the carriage rates and virulence genes of uropathogenic E. coli were equivalent based on culture. No correlation was found between E. coli, C. butyricum, and C. neonatale carriages, beta-lactam resistance, and antibiotic treatment. Conclusions: At disease onset, our data support a microbiota dysbiosis between NEC and control infants at the genus level. In addition, it provides valuable information on bacterial antimicrobial susceptibility. Full article

Necrotizing enterocolitis (NEC) is the most devastating gastrointestinal emergency in preterm neonates. Research on early predictive biomarkers is fundamental. This is a systematic review of studies applying untargeted metabolomics and gut microbiota analysis to evaluate the differences between neonates affected by NEC (Bell’s stage II or III), and/or by spontaneous intestinal perforation (SIP) versus healthy controls. Five studies applying metabolomics (43 cases, 95 preterm controls) and 20 applying gut microbiota analysis (254 cases, 651 preterm controls, 22 term controls) were selected. Metabolomic studies utilized NMR spectroscopy or mass spectrometry. An early urinary alanine/histidine ratio >4 showed good sensitivity and predictive value for NEC in one study. Samples collected in proximity to NEC diagnosis demonstrated variable pathways potentially related to NEC. In studies applying untargeted gut microbiota analysis, the sequencing of the V3–V4 or V3 to V5 regions of the 16S rRNA was the most used technique. At phylum level, NEC specimens were characterized by increased relative abundance of Proteobacteria compared to controls. At genus level, pre-NEC samples were characterized by a lack or decreased abundance of Bifidobacterium. Finally, at the species level Bacteroides dorei, Clostridium perfringens and perfringens-like strains dominated early NEC specimens, whereas Clostridium butyricum, neonatale and Propionibacterium acnei those at disease diagnosis. Six studies found a lower Shannon diversity index in cases than controls. A clear separation of cases from controls emerged based on UniFrac metrics in five out of seven studies. Importantly, no studies compared NEC versus SIP. Untargeted metabolomics and gut microbiota analysis are interrelated strategies to investigate NEC pathophysiology and identify potential biomarkers. Expression of quantitative measurements, data sharing via biorepositories and validation studies are fundamental to guarantee consistent comparison of results. Full article