Poster Session I - Poster of Distinction I - A21 DISRUPTION OF MUCIN-DERIVED SUGAR METABOLISM PATHWAYS IMPAIRS ENTERIC PATHOGEN CITROBACTER RODENTIUM COLONIZATION

作者：Z. Huang, M. Mslati, C. Ma, H. Yang, Q. Liang, S. Crowley, A. Gilliland, R. Dyer, I. Ng, H. Yu, B. Vallance, Experimental Medicine · 发表于：Journal of the Canadian Association of Gastroenterology · 年份：2026 · DOI：10.1093/jcag/gwaf042.021

Abstract Background Enteric bacterial pathogens within the Enterobacteriaceae family, including Escherichia coli and Salmonella species, can cause acute gastroenteritis in humans. In the competitive gastrointestinal environment, these pathogens depend on specific metabolic adaptations to establish infections. The intestinal mucus barrier, composed primarily of the mucin Muc2, protects the epithelium while also serving as a nutrient reservoir rich in host-derived monosaccharides such as N-acetylglucosamine (GlcNAc) and N-acetylneuraminic acid (NeuNAc). How these mucus-derived sugars are metabolized during infection and how dysregulation of these pathways affects bacterial pathogen fitness remain poorly understood. Aims We sought to determine how Enterobacteriaceae exploit mucin-derived sugars for colonization and whether disrupting these pathways impairs their fitness. Citrobacter rodentium, a murine-specific enteric pathogen, was used as a model system and was hypothesized to be able to exploit GlcNAc and NeuNAc to fuel their pathogenesis. Methods C. rodentium mutants were generated, including ΔnagA lacking GlcNAc-6P deacetylase, its complemented strain, and Δmana lacking GlcNAc/NeuNAc import systems. Colonization and tissue pathology were examined in C57BL/6J mice. Intracellular GlcNAc-6P was quantified by the Morgan–Elson assay. Transcriptional responses were analyzed by RT-qPCR. Bacterial susceptibility to cell wall stress was tested using lysozyme, osmotic, and antibiotic...