Endogenous carbohydrates released from the intestinal mucus represent a constant source of nutrients to the intestinal microbiota. Mucus‐derived carbohydrates can also be used as building blocks in the biosynthesis of bacterial cell wall components, thereby influencing host mucosal immunity. To assess the uptake of endogenous carbohydrates by gut microbes in healthy mice and during intestinal inflammation, we applied azido‐monosaccharides that can be tracked on bacterial cell walls after conjugation with fluorophores. In interleukin‐10 deficient mice, changes in the gut microbiota were accompanied by decreased carbohydrate hydrolase activities and increased lumenal concentrations of host glycan‐derived monosaccharides. Tracking of the monosaccharide N‐azidoacetylglucosamine (GlcNAz) in caecum bacteria revealed a preferential incorporation of this carbohydrate by Xanthomonadaceae in healthy mice and by Bacteroidaceae in interleukin‐10 deficient mice. These GlcNAz‐positive Bacteroidaceae fractions mainly belonged to the species B. acidifaciens and B. vulgatus. Growth of Bacteroides species in the presence of specific monosaccharides changed their stimulatory activity toward CD11c⁺ dendritic cells. Expression of activation markers and cytokine production was highest after stimulation of dendritic cells with B. vulgatus. The variable incorporation of monosaccharides by related Bacteroides species underline the necessity to investigate intestinal bacteria down to the species level when addressing microbiota‐host interactions.

中文翻译：

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肠道炎症改变粘膜碳水化合物觅食和单糖掺入微生物聚糖

从肠道粘液中释放的内源性碳水化合物代表了肠道微生物群的持续营养来源。粘液衍生的碳水化合物也可用作细菌细胞壁成分生物合成的构建块，从而影响宿主粘膜免疫。为了评估健康小鼠和肠道炎症期间肠道微生物对内源性碳水化合物的吸收，我们应用了叠氮基单糖，在与荧光团结合后可以在细菌细胞壁上进行追踪。在白细胞介素 10 缺陷小鼠中，肠道微生物群的变化伴随着碳水化合物水解酶活性的降低和宿主聚糖衍生单糖的腔内浓度增加。单糖N 的追踪盲肠细菌中的叠氮乙酰氨基葡萄糖 (GlcNAz) 表明，健康小鼠中的黄单胞菌科和白介素 10 缺陷小鼠中的拟杆菌科优先掺入这种碳水化合物。这些 GlcNAz 阳性的类杆菌科部分主要属于B. acidifaciens和B. vulgatus。在特定单糖存在下，拟杆菌属物种的生长改变了它们对 CD11c ⁺树突细胞的刺激活性。用普通芽孢杆菌刺激树突细胞后，活化标志物的表达和细胞因子的产生最高。相关联的单糖可变掺入在解决微生物群-宿主相互作用时，拟杆菌属物种强调了在物种水平上研究肠道细菌的必要性。