Mei Wang1, Min Li, Shuai Wu, Carlito B Lebrilla, Robert S Chapkin, Ivan Ivanov, Sharon M Donovan. 1. *Department of Food Science and Human Nutrition, University of Illinois, Urbana †Department of Chemistry, University of California, Davis ‡Program in Integrative Nutrition and Complex Diseases and Center for Environmental and Translational Health Research §Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station.
Abstract
OBJECTIVES: This study tested the hypothesis that the fecal bacterial genera of breast-fed (BF) and formula-fed (FF) infants differ and that human milk oligosaccharides (HMOs) modulate the microbiota of BF infants. METHODS: Fecal samples were obtained from BF (n = 16) or FF (n = 6) infants at 3-month postpartum. Human milk samples were collected on the same day when feces were collected. The microbiota was assessed by pyrosequencing of bacterial 16S ribosomal RNA genes. HMOs were measured by high-performance liquid chromatography-chip time-of-flight mass spectrometry. RESULTS: The overall microbiota of BF differed from that of FF (P = 0.005). Compared with FF, BF had higher relative abundances of Bacteroides, lower proportions of Clostridium XVIII, Lachnospiraceae incertae sedis, Streptococcus, Enterococcus, and Veillonella (P < 0.05). Bifidobacterium predominated in both BF and FF infants, with no difference in abundance between the 2 groups. The most abundant HMOs were lacto-N-tetraose + lacto-N-neotetraose (LNT + LNnT, 22.6%), followed by 2'-fucosyllactose (2'FL, 14.5%) and lacto-N-fucopentaose I (LNFP I, 9.5%). Partial least squares regression of HMO and microbiota showed several infant fecal bacterial genera could be predicted by their mothers' HMO profiles, and the important HMOs for the prediction of bacterial genera were identified by variable importance in the projection scores. CONCLUSIONS: These results strengthen the established relation between HMO and the infant microbiota and identify statistical means whereby infant bacterial genera can be predicted by milk HMO. Future studies are needed to validate these findings and determine whether the supplementation of formula with defined HMO could selectively modify the gut microbiota.
OBJECTIVES: This study tested the hypothesis that the fecal bacterial genera of breast-fed (BF) and formula-fed (FF) infants differ and that humanmilkoligosaccharides (HMOs) modulate the microbiota of BF infants. METHODS: Fecal samples were obtained from BF (n = 16) or FF (n = 6) infants at 3-month postpartum. Humanmilk samples were collected on the same day when feces were collected. The microbiota was assessed by pyrosequencing of bacterial 16S ribosomal RNA genes. HMOs were measured by high-performance liquid chromatography-chip time-of-flight mass spectrometry. RESULTS: The overall microbiota of BF differed from that of FF (P = 0.005). Compared with FF, BF had higher relative abundances of Bacteroides, lower proportions of Clostridium XVIII, Lachnospiraceae incertae sedis, Streptococcus, Enterococcus, and Veillonella (P < 0.05). Bifidobacterium predominated in both BF and FF infants, with no difference in abundance between the 2 groups. The most abundant HMOs were lacto-N-tetraose + lacto-N-neotetraose (LNT + LNnT, 22.6%), followed by 2'-fucosyllactose (2'FL, 14.5%) and lacto-N-fucopentaose I (LNFP I, 9.5%). Partial least squares regression of HMO and microbiota showed several infant fecal bacterial genera could be predicted by their mothers' HMO profiles, and the important HMOs for the prediction of bacterial genera were identified by variable importance in the projection scores. CONCLUSIONS: These results strengthen the established relation between HMO and the infant microbiota and identify statistical means whereby infant bacterial genera can be predicted by milk HMO. Future studies are needed to validate these findings and determine whether the supplementation of formula with defined HMO could selectively modify the gut microbiota.
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