Chronic obstructive pulmonary disease (COPD) is associated with colonization by bacterial pathogens and repeated airway infections, leading to exacerbations and impaired lung function. The highly glycosylated mucins in the mucus lining the airways are an important part of the host defense against pathogens. However, mucus accumulation can contribute to COPD pathology. Here, we examined whether inflammation is associated with glycosylation changes that affect interactions between airway mucins and pathogens. We isolated mucins from lower airway samples (n = 4–9) from long-term smokers with and without COPD and from never-smokers. The most abundant terminal glycan moiety was N-acetylneuraminic acid (Neu5Ac) among smokers with and without COPD and N-acetyl-hexoseamine among never-smokers. Moraxella catarrhalis bound to MUC5 mucins from smokers with and without COPD. M. catarrhalis binding correlated with inflammatory parameters and Neu5Ac content. M. catarrhalis binding was abolished by enzymatic removal of Neu5Ac. Furthermore, M. catarrhalis bound to α2,6 sialyl-lactose, suggesting that α2,6 sialic acid contributes to M. catarrhalis binding to mucins. Furthermore, we detected more M. catarrhalis binding to mucins from patients with pneumonia than to those from control subjects (n = 8–13), and this binding correlated with C-reactive protein and Neu5Ac levels. These results suggest a key role of inflammation-induced Neu5Ac in the adhesion of M. catarrhalis to airway mucins. The inflammation-induced ability of MUC5 mucins to bind M. catarrhalis is likely a host defense mechanism in the healthy lung, although it cannot be excluded that impaired mucociliary clearance limits the effectiveness of this defense in patients with COPD.

慢性阻塞性肺疾病 (COPD) 与细菌病原体定植和反复气道感染有关，导致病情恶化和肺功能受损。气道内壁粘液中高度糖基化的粘蛋白是宿主抵御病原体的重要组成部分。然而，粘液积累会导致 COPD 病理。在这里，我们检查了炎症是否与影响气道粘蛋白和病原体之间相互作用的糖基化变化有关。我们从 患有和不患有 COPD 的长期吸烟者和从不吸烟者的下呼吸道样本 ( n = 4–9) 中分离出粘蛋白。在患有和不患有 COPD 和N 的吸烟者中，最丰富的末端聚糖部分是N-乙酰神经氨酸 (Neu5Ac)-从不吸烟者中的乙酰己糖胺。卡他莫拉菌与患有和不患有 COPD 的吸烟者的 MUC5 粘蛋白结合。M. catarrhalis结合与炎症参数和 Neu5Ac 含量相关。通过酶促去除 Neu5Ac 消除了卡他莫氏菌的结合。此外，M. catarrhalis与 α2,6 唾液酸-乳糖结合，表明 α2,6 唾液酸有助于M. catarrhalis与粘蛋白结合。此外，我们检测到与肺炎患者粘蛋白结合的卡他分枝杆菌多于对照受试者的粘蛋白（n = 8–13)，并且这种结合与 C 反应蛋白和 Neu5Ac 水平相关。这些结果表明炎症诱导的 Neu5Ac 在卡他分枝杆菌粘附到气道粘蛋白中的关键作用。MUC5 粘蛋白结合卡他莫拉氏菌的炎症诱导能力可能是健康肺中的宿主防御机制，但不能排除黏液纤毛清除受损限制了这种防御在 COPD 患者中的有效性。