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Identification of a Pneumococcal Glycosidase That Modifies O-Linked Glycans

机译：修饰修饰O型糖链的肺炎球菌糖苷酶的鉴定

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Colonization of the airway by Streptococcus pneumoniae is typically asymptomatic; however, progression of bacteria beyond the oronasopharynx can cause diseases including otitis media and pneumonia. The mechanisms by which S. pneumoniae establishes and maintains colonization remain poorly understood. Both N-linked and O-linked glycans are abundant in the airway. Our previous research demonstrated that S. pneumoniae can sequentially deglycosylate N-linked glycans and suggested that this modification of sugar structures may aid in colonization. There is published evidence that S. pneumoniae expresses a secreted O-glycosidase that cleaves galactose β1-3 N-acetylgalactosamine (Galβ1-3GalNAc) from core-1 O-linked glycans; however, the biological function of this enzyme has not previously been determined. We established that the activity is not secreted but is instead surface associated in a sortase-dependent manner. Genome analysis revealed an open reading frame predicted to encode a sortase-dependent surface protein with sequence similarity to the O-glycosidase of Bifidobacterium longum. Deletion of this pneumococcal open reading frame confirmed that this gene encodes an O-glycosidase. Experiments using a model glycoconjugate demonstrated that this O-glycosidase, together with the neuraminidase NanA, is required for S. pneumoniae to cleave sialylated core-1 O-linked glycans. The ability of the O-glycosidase mutant to cleave this glycan structure was restored by both genetic complementation and the addition of O-glycosidase. The mutant showed a reduction in adherence to human airway epithelial cells and a significantly decreased ability to colonize the upper respiratory tract, suggesting that cleavage of core-1 O-linked glycans enhances the ability of S. pneumoniae to colonize the human airway.
机译：肺炎链球菌在气道中的定殖通常是无症状的。然而，口鼻咽部以外细菌的进展会引起包括中耳炎和肺炎在内的疾病。 S的机制。肺炎的建立和维持定植仍知之甚少。 N-连接和O-连接的聚糖在气道中都丰富。我们之前的研究表明 S。肺炎可以顺序地使N-连接的聚糖去糖基化，这表明糖结构的这种修饰可能有助于定殖。有公开证据表明， S。肺炎表达一种分泌的O-糖苷酶，可从核心1 O-连接的聚糖上裂解半乳糖β1-3 N -乙酰半乳糖胺（Galβ1-3GalNAc）。然而，该酶的生物学功能先前尚未确定。我们确定该活性不是分泌的，而是以分选酶依赖性的方式与表面相关。基因组分析揭示了一个开放阅读框，该框预计编码与长双歧杆菌的O-糖苷酶序列相似的排序酶依赖性表面蛋白。肺炎球菌开放阅读框的缺失证实该基因编码一个O-糖苷酶。使用模型糖缀合物的实验表明， S需要这种O-糖苷酶以及神经氨酸酶NanA。肺炎裂解唾液酸化的核心1 O-连接的聚糖。通过遗传互补和添加O-糖苷酶，恢复了O-糖苷酶突变体切割该聚糖结构的能力。该突变体显示出对人气道上皮细胞的粘附减少，并且在上呼吸道定殖的能力显着降低，表明核心-1 O-连接的聚糖的切割增强了 S的能力。肺炎定植于人类气道。

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