The glycosylation profile of the gastrointestinal tract is an important factor mediating host-microbe interactions. Variation in these glycan structures is often mediated by blood group-related glycosyltransferases, and can lead to wide-ranging differences in susceptibility to both infectious- as well as chronic disease. In this review, we focus on the interplay between host glycosylation, the intestinal microbiota and susceptibility to gastrointestinal pathogens based on studies of two exemplary blood group-related glycosyltransferases that are conserved between mice and humans, namely FUT2 and B4GALNT2. We highlight that differences in susceptibility can arise due to both changes in direct interactions, such as bacterial adhesion, as well as indirect effects mediated by the intestinal microbiota. Although a large body of experimental work exists for direct interactions between host and pathogen, determining the more complex and variable mechanisms underlying three-way interactions involving the intestinal microbiota will be the subject of much-needed future research.

胃肠道的糖基化谱是介导宿主-微生物相互作用的重要因素。这些聚糖结构的变异通常由血型相关的糖基转移酶介导，并可能导致对传染病和慢性疾病的易感性存在广泛差异。在这篇综述中，我们基于对小鼠和人类之间保守的两种示例性血型相关糖基转移酶（即FUT2和B4GALNT2）的研究，重点关注宿主糖基化、肠道微生物群和对胃肠道病原体易感性之间的相互作用。我们强调，易感性的差异可能是由于直接相互作用的变化（例如细菌粘附）以及肠道微生物群介导的间接影响而产生的。尽管宿主和病原体之间的直接相互作用存在大量实验工作，但确定涉及肠道微生物群的三向相互作用背后更复杂和多变的机制将是未来急需研究的主题。