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由EVC001亚种定殖的母乳喂养婴儿结肠黏蛋白降解减少。

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

作者信息

Karav Sercan, Casaburi Giorgio, Frese Steven A

机构信息

Department of Molecular Biology and Genetics Çanakkale Onsekiz Mart University Turkey.

Evolve Biosystems, Inc. Davis CA USA.

出版信息

FEBS Open Bio. 2018 Sep 17;8(10):1649-1657. doi: 10.1002/2211-5463.12516. eCollection 2018 Oct.

DOI:10.1002/2211-5463.12516
PMID:30338216
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6168692/
Abstract

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 and , but other bacteria, such as subsp, 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 EVC001 and from 10 infants colonized by higher levels of mucolytic taxa (controls), including , 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 -glycans from control infants composed 37.68% (± 3.14% SD) of the total glycan structure pool, whereas colonic mucin-derived -glycans made up of only 1.78% (± 0.038% SD) of the total in EVC001 samples. The relative abundance of these colonic mucin-derived -glycans in the total glycan pool was higher among control, 26.98% (± 8.48% SD), relative to colonized infants, 1.68% (± 1.12% SD). Key taxa, such as , were significantly and positively correlated with the abundance of these structures, while were significantly and negatively associated with these structures. These results suggest that colonization of infants by may diminish colonic glycan degradation and help maintain barrier function in the gastrointestinal tract of infants.

摘要

粘蛋白糖蛋白在保护肠道上皮方面发挥着重要作用,它使肠道微生物无法直接接触肠道上皮,同时允许小分子从肠腔扩散到上皮。粘蛋白糖萼可被诸如[具体细菌1]和[具体细菌2]等肠道细菌降解,但其他细菌,如[具体细菌3]亚种,则不能消耗粘蛋白聚糖。将非靶向质谱图谱与微生物组图谱进行比较,以评估不同的肠道微生物群如何影响结肠粘蛋白的降解。比较了从9名由EVC001定殖的婴儿和10名由更高水平的粘液溶解类群(对照组)定殖的婴儿(包括[具体细菌4])获得的样本。先前进行的非靶向纳米高效液相色谱芯片/飞行时间质谱用于检测和定量源自结肠粘蛋白的聚糖。对照组婴儿结肠粘蛋白衍生的[具体聚糖类型]聚糖占总聚糖结构库的37.68%(±3.14%标准差),而在EVC001样本中,结肠粘蛋白衍生的[具体聚糖类型]聚糖仅占总量的1.78%(±0.038%标准差)。在总聚糖库中,这些结肠粘蛋白衍生的[具体聚糖类型]聚糖的相对丰度在对照组中更高,为26.98%(±8.48%标准差),相对于定殖婴儿为1.68%(±1.12%标准差)。关键类群,如[具体细菌5],与这些结构的丰度呈显著正相关,而[具体细菌6]与这些结构呈显著负相关。这些结果表明,[具体细菌名称]对婴儿的定殖可能会减少结肠聚糖的降解,并有助于维持婴儿胃肠道的屏障功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e05d/6168692/25525680a43d/FEB4-8-1649-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e05d/6168692/43926b041d50/FEB4-8-1649-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e05d/6168692/5ff269144b27/FEB4-8-1649-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e05d/6168692/25525680a43d/FEB4-8-1649-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e05d/6168692/43926b041d50/FEB4-8-1649-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e05d/6168692/5ff269144b27/FEB4-8-1649-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e05d/6168692/25525680a43d/FEB4-8-1649-g003.jpg

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