Mucin-Pseudomonas aeruginosa interactions promote biofilm formation and antibiotic resistance
Mucin-Pseudomonas aeruginosa interactions promote biofilm formation and antibiotic resistance
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DOI：
10.1111/j.1365-2958.2005.04941.x
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发表时间：
2006-01-01
影响因子：
3.6
通讯作者：
Parsek, MR
中科院分区：
文献类型：
--
作者：
Landry, RM;An, DD;Parsek, MR
铜绿假单胞菌是一种机会致病菌，可引起囊性纤维化（CF）患者的慢性肺部感染。在CF气道中，铜绿假单胞菌形成称为生物膜的表面相关群落。与自由游动培养物相比，生物膜抵抗宿主免疫系统的清除，并显示出对抗菌剂的耐药性增加。在这项研究中，我们开发了一种技术，用CF气道中丰富的分子涂覆表面，以研究它们对铜绿假单胞菌生物膜发育的影响。我们发现，铜绿假单胞菌生物膜的发展进行不同的表面上的糖蛋白粘蛋白包被的生物膜的发展相比，玻璃和表面上的肌动蛋白或DNA包被。粘蛋白涂层表面上形成的生物膜开发大的细胞聚集体，并增加了耐受性的抗生素妥布霉素相比，在玻璃上生长的生物膜。结合延时显微镜分析选定的突变体背景显示，粘蛋白表面上的表面相关的运动被阻止。此外，我们的数据表明，特定的粘附素-粘蛋白相互作用将细菌固定在表面上。总之，这些实验表明，粘蛋白，其可以作为CF气道中的附着表面，影响铜绿假单胞菌生物膜的发展和功能。
Pseudomonas aeruginosa is an opportunistic pathogen that causes chronic lung infections in people suffering from cystic fibrosis (CF). In CF airways, P. aeruginosa forms surface-associated communities called biofilms. Compared with free-swimming cultures, biofilms resist clearance by the host immune system and display increased resistance to antimicrobial agents. In this study we developed a technique to coat surfaces with molecules that are abundant in CF airways in order to investigate their impact on P. aeruginosa biofilm development. We found that P. aeruginosa biofilm development proceeds differently on surfaces coated with the glycoprotein mucin compared with biofilm development on glass and surfaces coated with actin or DNA. Biofilms formed on mucin-coated surfaces developed large cellular aggregates and had increased tolerance to the antibiotic tobramycin compared with biofilms grown on glass. Analysis of selected mutant backgrounds in conjunction with time-lapse microscopy revealed that surface-associated motility was blocked on the mucin surface. Furthermore, our data suggest that a specific adhesin-mucin interaction immobilizes the bacterium on the surface. Together, these experiments suggest that mucin, which may serve as an attachment surface in CF airways, impacts P. aeruginosa biofilm development and function.