Carbohydrate sulfation effects on growth of Pseudomonas aeruginosa
Carbohydrate sulfation effects on growth of Pseudomonas aeruginosa
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DOI：
10.1099/00221287-146-7-1717
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发表时间：
2000-07-01
期刊：
影响因子：
--
通讯作者：
Mawhinney, TP
中科院分区：
文献类型：
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作者：
Chance, DL;Mawhinney, TP
铜绿假单胞菌是囊性纤维化的病理和发病率的关键因素，囊性纤维化是慢性阻塞性肺疾病，由这种遗传疾病最常见和最严重的突变引起，通常包括铜绿假单胞菌慢性感染，即使使用坚固的抗生素和物理治疗方案，也很少能根除。目前尚不清楚囊性纤维化气管-支气管壁粘蛋白的低聚糖硫化特性是否在铜绿假单胞菌在呼吸道中的存活中起作用，本研究合成了硫化单糖，并在体外测试了它们作为唯一碳源对该菌临床分离株和实验室菌株生长的影响。观察到碳水化合物的硫酸盐化可以减少但不是阻止铜绿假单胞菌在通常以非硫酸盐形式利用的碳水化合物上的生长。作为唯一碳源的各种硫酸盐糖提供了特征一致的生长曲线和所测试菌株的最大生长值。囊性纤维化患者的铜绿假单胞菌分离株通常表现为粘液表型，这被认为有助于它们在恶劣条件下生存。碳水化合物硫化对生长的影响在粘液型和非粘液型菌株之间没有显著差异。这些结果表明，囊性纤维化中记录的气管、支气管粘蛋白的额外硫酸盐化实际上可能有助于粘蛋白对铜绿假单胞菌和潜在的其他病原体的利用，提供额外的宿主保护水平，并限制可用营养库，从而限制细菌的生长。
Pseudomonas aeruginosa is a key player in the pathology and morbidity of cystic fibrosis, Chronic obstructive pulmonary disease, which results from the most common and severe mutations in this genetic disorder, typically includes chronic infection with P. aeruginosa which, even with rugged antibiotic and physical therapy regimens, is rarely eradicated. it is not known whether the increased oligosaccharide sulfation characteristic of cystic fibrosis tracheobronchial mucins plays a role in the survival of P, aeruginosa in the airway, In this study, sulfated monosaccharides were synthesized and tested for their effects on the growth of clinical isolates and laboratory strains of this organism when supplied as the sole carbon source in vitro. Carbohydrate sulfation was observed to reduce, but not prohibit, growth of P, aeruginosa on carbohydrates normally utilized in their nonsulfated form. The various sulfated sugars employed as the sole carbon source gave characteristic and consistent growth profiles and maximum growth values across the strains tested. P, aeruginosa isolates from patients with cystic fibrosis often express a mucoid phenotype, which is thought to contribute to their ability to survive in harsh conditions. Carbohydrate sulfation effects on growth did not differ significantly between mucoid and nonmucoid strains. These results suggest that the additional sulfation of tracheobronchial mucin documented in cystic fibrosis may in fact contribute to the mucin's resistance to utilization by P. aeruginosa and potentially other pathogens, providing an additional level of host protection, and limiting the available nutrient pool and thereby bacterial growth.