Mucosal surfaces are colonized by highly diverse commensal microbiota. Coating with secretory IgA (SIgA) promotes the survival of commensal bacteria while it inhibits the invasion by pathogens. Bacterial coating could be mediated by antigen-specific SIgA recognition, polyreactivity, and/or by the SIgA-associated glycans. In contrast to many in vitro studies, only a few reported the effect of SIgA glycans in vivo. Here, we used a germ-free antibody-free newborn piglets model to compare the protective effect of SIgA, SIgA with enzymatically removed N-glycans, Fab, and Fc containing the secretory component (Fc-SC) during oral necrotoxigenic E. coli O55 challenge. SIgA, Fab, and Fc-SC were protective, whereas removal of N-glycans from SIgA reduced SIgA-mediated protection as demonstrated by piglets’ intestinal histology, clinical status, and survival. In vitro analyses indicated that deglycosylation of SIgA did not reduce agglutination of E. coli O55. These findings highlight the role of SIgA-associated N-glycans in protection. Further structural studies of SIgA-associated glycans would lead to the identification of those involved in the species-specific inhibition of attachment to corresponding epithelial cells.

粘膜表面被高度多样化的共生微生物群定殖。涂有分泌型 IgA (SIgA) 可促进共生细菌的存活，同时抑制病原体的入侵。细菌涂层可由抗原特异性 SIgA 识别、多反应性和/或 SIgA 相关聚糖介导。与许多体外研究相反，只有少数研究报告了 SIgA 聚糖在体内的作用。在这里，我们使用无菌无抗体的新生仔猪模型来比较 SIgA、SIgA 与酶法去除的N-聚糖、Fab 和含有分泌成分 (Fc-SC) 的 Fc 在口腔坏死性产毒素大肠杆菌O55期间的保护作用挑战。SIgA、Fab 和 Fc-SC 具有保护作用，而去除N来自 SIgA 的聚糖降低了 SIgA 介导的保护作用，如仔猪的肠道组织学、临床状态和存活率所示。体外分析表明 SIgA 的去糖基化不会降低大肠杆菌O55 的凝集。这些发现突出了 SIgA 相关N-聚糖在保护中的作用。对 SIgA 相关聚糖的进一步结构研究将导致鉴定那些参与物种特异性抑制附着到相应上皮细胞的聚糖。