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Sensitizing bacterial cells to antibiotics by shape recovery triggered biofilm dispersion

机译:通过形状恢复触发生物膜分散使细菌细胞对抗生素敏感

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摘要

Microbial biofilms are a leading cause of chronic infections in humans and persistent biofouling in industries due to extremely high-level tolerance of biofilm cells to antimicrobial agents. Eradicating mature biofilms is especially challenging because of the protection of the extracellular matrix and slow growth of biofilm cells. Recently, we reported that established biofilms can be effectively removed (e.g. 99.9% dispersion of 48 h Pseudomonas aeruginosa PAO1 biofilms) by shape memory polymer-based dynamic changes in surface topography. Here, we demonstrate that such biofilm dispersion also sensitizes biofilm cells to conventional antibiotics. For example, shape recovery in the presence of 50 µg/mL tobramycin reduced biofilm cell counts by more than 3 logs (2,479-fold) compared to the static flat control. The observed effects were attributed to the disruption of biofilm structure and increase in cellular activities as evidenced by an 11.8-fold increase in intracellular level of adenosine triphosphate (ATP), and 4.1-fold increase in expression of the rrnB gene in detached cells. These results can help guide the design of new control methods to better combat biofilm associated antibiotic-resistant infections.
机译:由于生物膜细胞对抗菌剂的极高耐受性,微生物生物膜是人类慢性感染和工业持续性生物污染的主要原因。由于细胞外基质的保护和生物膜细胞的缓慢生长,根除成熟的生物膜尤其具有挑战性。最近,我们报道了通过基于形状记忆聚合物的表面形貌动态变化,可以有效地去除已建立的生物膜(例如48 h铜绿假单胞菌PAO1生物膜的99.9%分散度)。在这里,我们证明了这种生物膜的分散也使生物膜细胞对常规抗生素敏感。例如,与静态平板对照组相比,在存在50 µg / mL妥布霉素的情况下,形状恢复可使生物膜细胞计数减少3倍以上(2,479倍)。观察到的影响归因于生物膜结构的破坏和细胞活性的增加,如三磷酸腺苷(ATP)的细胞内水平增加了11.8倍,而分离细胞中rrnB基因的表达增加了4.1倍。这些结果可以帮助指导设计新的控制方法,以更好地抵抗生物膜相关的抗生素耐药性感染。

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