Pseudomonas aeruginosa mucoid strain 8830 binds glycans containing the sialyl-Lewis x epitope.
Pseudomonas aeruginosa mucoid strain 8830 binds glycans containing the sialyl-Lewis x epitope.
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铜绿假单胞菌粘液菌株 8830 结合含有唾液酸-Lewis x 表位的聚糖。
DOI：
10.1007/s10719-006-9015-y
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发表时间：
2007
影响因子：
3
通讯作者：
Cummings,RichardD
中科院分区：
文献类型：
--
作者：
Xia,Baoyun;Sachdev,GoverdhanP;Cummings,RichardD
囊性纤维化（CF）患者的铜绿假单胞菌感染是其发病率和死亡率的主要原因。发病机制部分是由P.呼吸道粘蛋白中的碳水化合物残留物在患有这种疾病的患者的肺中积累。探索稳定的、粘液样的、产生藻酸盐的菌株P所识别的聚糖的性质。我们用Pa 3380-GFP转化AERCOLOSA 8830，产生了表达绿色荧光蛋白（Pa 3380-GFP）的遗传修饰的Pa 8830。我们测试了其结合的糖脂和neoglycolipids，其中选定的聚糖共价连接到二棕榈酰磷脂酰乙醇胺和硅胶表面上进行分析的面板。在所有检测的聚糖中，Pa 8830-GFP与含唾液酸-Lex的聚糖NeuAc（α2-3）Gal（β1-4）[Fuc（α1-3）]GlcNAc-R的结合最好，与H型血型Fucα1-2Galβ1-4GlcNAc-R、唾液酸-乳糖和Lex的结合较弱，与非岩藻糖基化衍生物的结合很少。有趣的是，虽然Pa 8830-GFP与鞘糖脂脱唾液酸GM 1结合，但它似乎不与各种其他鞘糖脂结合，包括GM 1、GM 2、脱唾液酸GM 2和硫苷脂。这些结果表明P. aerodecosa 8830优先结合含唾液酸Lex的聚糖，对相关的含岩藻糖和唾液酸的聚糖识别较弱。Pa 8830结合CF患者粘蛋白中含量增加的含唾液酸Lex聚糖的发现与其他P菌株的研究一致。aerodyniae和进一步表明，CF粘蛋白上的这种聚糖有助于疾病的发病机制。
Pseudomonas aeruginosainfection of patients with cystic fibrosis (CF) is a leading cause of their morbidity and mortality. Pathogenesis is initiated in part by molecular interactions ofP. aeruginosawith carbohydrate residues in airway mucins that accumulate in the lungs of patients with this disease. To explore the nature of the glycans recognized by a stable, mucoid, alginate-producing strainP. aeruginosa8830 we generated a genetically modified Pa8830 expressing green fluorescent protein (Pa3380-GFP). We tested its binding to a panel of glycolipids and neoglycolipids in which selected glycans were covalently attached to dipalmitoyl phosphatidylethanolamine and analyzed on silica gel surfaces. Among all glycans tested, Pa8830-GFP bound best to sialyl-Lex-containing glycan NeuAc(α2-3)Gal(β1-4)[Fuc(α1-3)]GlcNAc-R and bound weakly to H-type blood group Fucα1-2Galβ1-4GlcNAc-R, sialyl-lactose, and Lex, and exhibited little binding toward non-fucosylated derivatives. Interestingly, while Pa8830-GFP bound to the glycosphingolipid asialoGM1, it did not appear to bind to a wide variety of other glycosphingolipids including GM1, GM2, asialoGM2, and sulfatide. These results indicate thatP. aeruginosa8830 has preferential binding to sialyl-Lex-containing glycans and has weak recognition of related fucose- and sialic acid-containing glycans. The finding that Pa8830 binds sialyl-Lex-containing glycans, which occur at increased levels in mucins from CF patients, is consistent with studies of other strains ofP. aeruginosaand further suggests that such glycans on CF mucins contribute to disease pathogenesis.