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

Sercan Karav, Giorgio Casaburi, Steven A Frese, Sercan Karav, Giorgio Casaburi, Steven A Frese

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 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.

Keywords: Bacteroides; Bifidobacterium infantis; glycome; mucin; mucinlike glycans.

Figures

Figure 1
Figure 1
(A) The relative abundance of the taxa, as reported at the family level by Frese et al. 2017, of each fecal sample in this analysis. (B) PCoA of the gut microbiome at the family level; control (CON) samples are shown as gray points, and EVC001‐fed infant samples are shown as teal points. 87.5% of total variation was described in the first two principal components (PC1 and PC2). PERMANOVA comparisons identified a significant difference between the two treatment groups by composition (= 26.5, = 0.001).
Figure 2
Figure 2
Comparison of fecal glycome and colonic mucin‐derived O‐glycans of control and EVC001‐fed infant feces. (A) Total number of OS detected across treatment groups. (B) Number of colonic mucin‐derived O‐glycans across treatment groups. (C) Relative abundance of the total number of colonic mucin‐derived O‐glycans in the total OS pool across treatment groups. (D) Percent of the OS assigned to colonic mucin‐derived O‐glycans in the total OS abundance across treatment groups.
Figure 3
Figure 3
PCoA of colonic mucin‐derived O‐glycan composition among samples using a Bray–Curtis dissimilarity index; control (Con) samples are shown as gray points, and EVC001‐fed infant samples are shown as teal points. 63.3% of total variation was explained in the first two principal components (PC1 and PC2). PERMANOVA comparisons identified a significant difference between the two groups, with respect to colonic mucin‐derived O‐glycan composition (R = 12.4; = 0.001).

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Source: PubMed

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