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Human milk glycomics and gut microbial genomics in infant feces show a correlation between human milk oligosaccharides and gut microbiota: a proof-of-concept study.

De Leoz ML, Kalanetra KM, Bokulich NA, Strum JS, Underwood MA, German JB, Mills DA, Lebrilla CB - J. Proteome Res. (2014)

Bottom Line: This was followed by decreases in fecal HMOs as the proportion of HMO-consuming Bacteroidaceae and Bifidobacteriaceae increased.These results represent a proof-of-concept and are consistent with the highly selective, prebiotic effect of HMOs in shaping the gut microbiota in the first weeks of life.The analysis of selective fecal bacterial substrates as a measure of alterations in the gut microbiota may be a potential marker of dysbiosis.

View Article: PubMed Central - PubMed

Affiliation: Departments of Chemistry, ‡Viticulture and Enology, §Food Science and Technology, ∥Pediatrics, and ⊥Biochemistry, #Foods for Health Institute, University of California Davis , One Shields Avenue, Davis, California 95616, United States.

ABSTRACT
Human milk oligosaccharides (HMOs) play a key role in shaping and maintaining a healthy infant gut microbiota. This article demonstrates the potential of combining recent advances in glycomics and genomics to correlate abundances of fecal microbes and fecal HMOs. Serial fecal specimens from two healthy breast-fed infants were analyzed by bacterial DNA sequencing to characterize the microbiota and by mass spectrometry to determine abundances of specific HMOs that passed through the intestinal tract without being consumed by the luminal bacteria. In both infants, the fecal bacterial population shifted from non-HMO-consuming microbes to HMO-consuming bacteria during the first few weeks of life. An initial rise in fecal HMOs corresponded with bacterial populations composed primarily of non-HMO-consuming Enterobacteriaceae and Staphylococcaeae. This was followed by decreases in fecal HMOs as the proportion of HMO-consuming Bacteroidaceae and Bifidobacteriaceae increased. Analysis of HMO structures with isomer differentiation revealed that HMO consumption is highly structure-specific, with unique isomers being consumed and others passing through the gut unaltered. These results represent a proof-of-concept and are consistent with the highly selective, prebiotic effect of HMOs in shaping the gut microbiota in the first weeks of life. The analysis of selective fecal bacterial substrates as a measure of alterations in the gut microbiota may be a potential marker of dysbiosis.

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Changes in oligosaccharide intensitiesand bacterial populationin the feces of Infant B. (A) Percent change in H/D ratios of HMOsin the feces of Infant B at weeks 0, 1, 2, and 14. Intensities wereobtained using MALDI FT-ICR MS in (+) ion mode with n = 3. H/D ratios were normalized to week 0, set at 100%. Each barrepresents an oligosaccharide nominal mass. (B) Corresponding fecalbacterial population of Infant B using 16S rDNA pyrosequencing.
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fig4: Changes in oligosaccharide intensitiesand bacterial populationin the feces of Infant B. (A) Percent change in H/D ratios of HMOsin the feces of Infant B at weeks 0, 1, 2, and 14. Intensities wereobtained using MALDI FT-ICR MS in (+) ion mode with n = 3. H/D ratios were normalized to week 0, set at 100%. Each barrepresents an oligosaccharide nominal mass. (B) Corresponding fecalbacterial population of Infant B using 16S rDNA pyrosequencing.

Mentions: A second infant, InfantB, also shows development of a saccharolytic microbiota. Figure 4A,B shows the glycoprofiles (analyzed by MALDI FT-ICRMS) and bacterial populations (analyzed by 16S rDNA pyrosequencing)over the infant’s first 14 weeks of life, respectively. Weobserve the fecal glycans to increase dramatically from week 0 toweek 1. Note that the y axis in this figure is logarithmicand that the increases vary from 14-fold to >1 million-fold. Atweek2, there is little change in HMO abundance in the feces, whereas atweek 14, all of the measured fecal HMOs have decreased (range 2-foldto 7000-fold higher than baseline).


Human milk glycomics and gut microbial genomics in infant feces show a correlation between human milk oligosaccharides and gut microbiota: a proof-of-concept study.

De Leoz ML, Kalanetra KM, Bokulich NA, Strum JS, Underwood MA, German JB, Mills DA, Lebrilla CB - J. Proteome Res. (2014)

Changes in oligosaccharide intensitiesand bacterial populationin the feces of Infant B. (A) Percent change in H/D ratios of HMOsin the feces of Infant B at weeks 0, 1, 2, and 14. Intensities wereobtained using MALDI FT-ICR MS in (+) ion mode with n = 3. H/D ratios were normalized to week 0, set at 100%. Each barrepresents an oligosaccharide nominal mass. (B) Corresponding fecalbacterial population of Infant B using 16S rDNA pyrosequencing.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4286166&req=5

fig4: Changes in oligosaccharide intensitiesand bacterial populationin the feces of Infant B. (A) Percent change in H/D ratios of HMOsin the feces of Infant B at weeks 0, 1, 2, and 14. Intensities wereobtained using MALDI FT-ICR MS in (+) ion mode with n = 3. H/D ratios were normalized to week 0, set at 100%. Each barrepresents an oligosaccharide nominal mass. (B) Corresponding fecalbacterial population of Infant B using 16S rDNA pyrosequencing.
Mentions: A second infant, InfantB, also shows development of a saccharolytic microbiota. Figure 4A,B shows the glycoprofiles (analyzed by MALDI FT-ICRMS) and bacterial populations (analyzed by 16S rDNA pyrosequencing)over the infant’s first 14 weeks of life, respectively. Weobserve the fecal glycans to increase dramatically from week 0 toweek 1. Note that the y axis in this figure is logarithmicand that the increases vary from 14-fold to >1 million-fold. Atweek2, there is little change in HMO abundance in the feces, whereas atweek 14, all of the measured fecal HMOs have decreased (range 2-foldto 7000-fold higher than baseline).

Bottom Line: This was followed by decreases in fecal HMOs as the proportion of HMO-consuming Bacteroidaceae and Bifidobacteriaceae increased.These results represent a proof-of-concept and are consistent with the highly selective, prebiotic effect of HMOs in shaping the gut microbiota in the first weeks of life.The analysis of selective fecal bacterial substrates as a measure of alterations in the gut microbiota may be a potential marker of dysbiosis.

View Article: PubMed Central - PubMed

Affiliation: Departments of Chemistry, ‡Viticulture and Enology, §Food Science and Technology, ∥Pediatrics, and ⊥Biochemistry, #Foods for Health Institute, University of California Davis , One Shields Avenue, Davis, California 95616, United States.

ABSTRACT
Human milk oligosaccharides (HMOs) play a key role in shaping and maintaining a healthy infant gut microbiota. This article demonstrates the potential of combining recent advances in glycomics and genomics to correlate abundances of fecal microbes and fecal HMOs. Serial fecal specimens from two healthy breast-fed infants were analyzed by bacterial DNA sequencing to characterize the microbiota and by mass spectrometry to determine abundances of specific HMOs that passed through the intestinal tract without being consumed by the luminal bacteria. In both infants, the fecal bacterial population shifted from non-HMO-consuming microbes to HMO-consuming bacteria during the first few weeks of life. An initial rise in fecal HMOs corresponded with bacterial populations composed primarily of non-HMO-consuming Enterobacteriaceae and Staphylococcaeae. This was followed by decreases in fecal HMOs as the proportion of HMO-consuming Bacteroidaceae and Bifidobacteriaceae increased. Analysis of HMO structures with isomer differentiation revealed that HMO consumption is highly structure-specific, with unique isomers being consumed and others passing through the gut unaltered. These results represent a proof-of-concept and are consistent with the highly selective, prebiotic effect of HMOs in shaping the gut microbiota in the first weeks of life. The analysis of selective fecal bacterial substrates as a measure of alterations in the gut microbiota may be a potential marker of dysbiosis.

Show MeSH