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Reduced colonic mucin degradation in breastfed infants colonized by Bifidobacterium longum subsp. infantis EVC001

Mucin glycoproteins play an important role in protecting the gut epithelium by keeping gut microbes from direct contact with the gut epithelium while allowing for diffusion of small molecules from the lumen to the epithelium. The mucin glycocalyx can be degraded by gut bacteria such as Bacteroides a...

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Autores principales: Karav, Sercan, Casaburi, Giorgio, Frese, Steven A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6168692/
https://www.ncbi.nlm.nih.gov/pubmed/30338216
http://dx.doi.org/10.1002/2211-5463.12516
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author Karav, Sercan
Casaburi, Giorgio
Frese, Steven A.
author_facet Karav, Sercan
Casaburi, Giorgio
Frese, Steven A.
author_sort Karav, Sercan
collection PubMed
description Mucin glycoproteins play an important role in protecting the gut epithelium by keeping gut microbes from direct contact with the gut epithelium while allowing for diffusion of small molecules from the lumen to the epithelium. The mucin glycocalyx can be degraded by gut bacteria such as Bacteroides and Akkermansia, but other bacteria, such as Bifidobacterium longum subsp. Infantis, cannot consume mucin glycans. Untargeted mass spectrometry profiles were compared to microbiome profiles to assess how different gut microbiomes affect colonic mucin degradation. Samples obtained from nine infants colonized by Bifidobacterium infantis EVC001 and from 10 infants colonized by higher levels of mucolytic taxa (controls), including Bacteroides, were compared. Previously performed untargeted nano‐high‐performance liquid chromatography‐chip/time‐of‐flight mass spectrometry was used to detect and quantify glycans originating from colonic mucin. Colonic mucin‐derived O‐glycans from control infants composed 37.68% (± 3.14% SD) of the total glycan structure pool, whereas colonic mucin‐derived O‐glycans made up of only 1.78% (± 0.038% SD) of the total in B. infantis EVC001 samples. The relative abundance of these colonic mucin‐derived O‐glycans in the total glycan pool was higher among control, 26.98% (± 8.48% SD), relative to B. infantis‐colonized infants, 1.68% (± 1.12% SD). Key taxa, such as Bacteroidaceae, were significantly and positively correlated with the abundance of these structures, while Bifidobacteriaceae were significantly and negatively associated with these structures. These results suggest that colonization of infants by B. infantis may diminish colonic glycan degradation and help maintain barrier function in the gastrointestinal tract of infants.
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spelling pubmed-61686922018-10-18 Reduced colonic mucin degradation in breastfed infants colonized by Bifidobacterium longum subsp. infantis EVC001 Karav, Sercan Casaburi, Giorgio Frese, Steven A. FEBS Open Bio Research Articles Mucin glycoproteins play an important role in protecting the gut epithelium by keeping gut microbes from direct contact with the gut epithelium while allowing for diffusion of small molecules from the lumen to the epithelium. The mucin glycocalyx can be degraded by gut bacteria such as Bacteroides and Akkermansia, but other bacteria, such as Bifidobacterium longum subsp. Infantis, cannot consume mucin glycans. Untargeted mass spectrometry profiles were compared to microbiome profiles to assess how different gut microbiomes affect colonic mucin degradation. Samples obtained from nine infants colonized by Bifidobacterium infantis EVC001 and from 10 infants colonized by higher levels of mucolytic taxa (controls), including Bacteroides, were compared. Previously performed untargeted nano‐high‐performance liquid chromatography‐chip/time‐of‐flight mass spectrometry was used to detect and quantify glycans originating from colonic mucin. Colonic mucin‐derived O‐glycans from control infants composed 37.68% (± 3.14% SD) of the total glycan structure pool, whereas colonic mucin‐derived O‐glycans made up of only 1.78% (± 0.038% SD) of the total in B. infantis EVC001 samples. The relative abundance of these colonic mucin‐derived O‐glycans in the total glycan pool was higher among control, 26.98% (± 8.48% SD), relative to B. infantis‐colonized infants, 1.68% (± 1.12% SD). Key taxa, such as Bacteroidaceae, were significantly and positively correlated with the abundance of these structures, while Bifidobacteriaceae were significantly and negatively associated with these structures. These results suggest that colonization of infants by B. infantis may diminish colonic glycan degradation and help maintain barrier function in the gastrointestinal tract of infants. John Wiley and Sons Inc. 2018-09-17 /pmc/articles/PMC6168692/ /pubmed/30338216 http://dx.doi.org/10.1002/2211-5463.12516 Text en © 2018 The Authors. Published by FEBS Press and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Articles
Karav, Sercan
Casaburi, Giorgio
Frese, Steven A.
Reduced colonic mucin degradation in breastfed infants colonized by Bifidobacterium longum subsp. infantis EVC001
title Reduced colonic mucin degradation in breastfed infants colonized by Bifidobacterium longum subsp. infantis EVC001
title_full Reduced colonic mucin degradation in breastfed infants colonized by Bifidobacterium longum subsp. infantis EVC001
title_fullStr Reduced colonic mucin degradation in breastfed infants colonized by Bifidobacterium longum subsp. infantis EVC001
title_full_unstemmed Reduced colonic mucin degradation in breastfed infants colonized by Bifidobacterium longum subsp. infantis EVC001
title_short Reduced colonic mucin degradation in breastfed infants colonized by Bifidobacterium longum subsp. infantis EVC001
title_sort reduced colonic mucin degradation in breastfed infants colonized by bifidobacterium longum subsp. infantis evc001
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6168692/
https://www.ncbi.nlm.nih.gov/pubmed/30338216
http://dx.doi.org/10.1002/2211-5463.12516
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