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A genetic basis for Pseudomonas aeruginosa biofilm antibiotic resistance

机译：铜绿假单胞菌生物膜抗生素抗性的遗传基础

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摘要

Biofilms are surface-attached microbial communities with characteristic architecture and phenotypic and biochemical properties distinct from their free-swimming, planktonic counterparts. One of the best-known of these biofilm-specific properties is the development of antibiotic resistance that can be up to 1,000-fold greater than planktonic cells. We report a genetic determinant of this high-level resistance in the Gram-negative opportunistic pathogen, Pseudomonas aeruginosa. We have identified a mutant of P. aeruginosa that, while still capable of forming biofilms with the characteristic P. aeruginosa architecture, does not develop high-level biofilm-specific resistance to three different classes of antibiotics. The locus identified in our screen, ndvB, is required for the synthesis of periplasmic glucans. Our discovery that these periplasmic glucans interact physically with tobramycin suggests that these glucose polymers may prevent antibiotics from reaching their sites of action by sequestering these antimicrobial agents in the periplasm. Our results indicate that biofilms themselves are not simply a diffusion barrier to these antibiotics, but rather that bacteria within these microbial communities employ distinct mechanisms to resist the action of antimicrobial agents.
机译：生物膜是表面附着的微生物群落，具有独特的结构，表型和生化特性，与自由游动的浮游生物不同。这些生物膜特有的特性中最著名的一种是对抗生素的抵抗力的发展，这种抗药性可能是浮游细胞的1000倍。我们报告了在革兰氏阴性机会性病原体铜绿假单胞菌中这种高水平抗药性的遗传决定因素。我们已经鉴定出一种铜绿假单胞菌的突变体，尽管它仍然能够形成具有特征性的铜绿假单胞菌结构的生物膜，但对三类不同的抗生素没有产生高水平的生物膜特异性抗性。在我们的筛查中确定的位点ndvB是合成周质葡聚糖所必需的。我们发现这些周质葡聚糖与妥布霉素发生物理相互作用，这表明这些葡萄糖聚合物可以通过将这些抗微生物剂隔离在周质中来阻止抗生素到达其作用部位。我们的结果表明，生物膜本身不仅是这些抗生素的扩散屏障，而且这些微生物群落中的细菌采用独特的机制来抵抗抗菌剂的作用。

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