首页> 美国卫生研究院文献>Wiley-Blackwell Online Open >Reduced colonic mucin degradation in breastfed infants colonized by Bifidobacterium longum subsp. infantis EVC001
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Reduced colonic mucin degradation in breastfed infants colonized by Bifidobacterium longum subsp. infantis EVC001

机译:减少了由长双歧杆菌亚种定殖的母乳喂养婴儿的结肠粘蛋白降解。婴儿EVC001

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摘要

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.
机译:粘蛋白糖蛋白通过防止肠道微生物直接与肠道上皮接触,同时允许小分子从管腔扩散到上皮,在保护肠道上皮中起重要作用。粘蛋白糖萼可以被肠道细菌(例如拟杆菌和阿克曼虫)降解,但其他细菌(例如长双歧杆菌亚种)则可以降解。婴儿,不能食用粘蛋白聚糖。将非靶向质谱图与微生物组图进行比较,以评估不同的肠道微生物群如何影响结肠粘蛋白降解。比较了从婴儿双歧杆菌EVC001定居的9例婴儿和通过更高水平的粘液溶解类群(对照)定居的10例婴儿(包括拟杆菌)的样品。以前执行的非靶向纳米高效液相色谱芯片/飞行时间质谱仪用于检测和定量源自结肠粘蛋白的聚糖。对照婴儿的结肠粘蛋白来源的O-聚糖占总糖结构池的37.68%(±3.14%SD),而结肠粘液来源的O-聚糖仅占总糖结构池的1.78%(±0.038%SD)。 B.infantis EVC001样品。这些结肠粘蛋白来源的O-聚糖在总聚糖库中的相对丰度在对照组中较高,为26.98%(±8.48%SD),相对于婴儿范氏定殖婴儿为1.68%(±1.12%SD)。关键类群(如拟杆菌科)与这些结构的丰度显着正相关,而双歧杆菌科则与这些结构显着正相关。这些结果表明,婴儿双歧杆菌定植婴儿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。

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