Li Xiaobao, Lu Nanxi, Brady Hannah R, Packman Aaron I
Department of Civil and Environmental Engineering, Northwestern University, Evanston, Illinois, USA.
Department of Civil and Environmental Engineering, Northwestern University, Evanston, Illinois, USA
Antimicrob Agents Chemother. 2016 Apr 22;60(5):2993-3000. doi: 10.1128/AAC.00203-16. Print 2016 May.
Ureolytic biomineralization induced by urease-producing bacteria, particularly Proteus mirabilis, is responsible for the formation of urinary tract calculi and the encrustation of indwelling urinary catheters. Such microbial biofilms are challenging to eradicate and contribute to the persistence of catheter-associated urinary tract infections, but the mechanisms responsible for this recalcitrance remain obscure. In this study, we characterized the susceptibility of wild-type (ure+) and urease-negative (ure-) P. mirabilis biofilms to killing by ciprofloxacin. Ure+ biofilms produced fine biomineral precipitates that were homogeneously distributed within the biofilm biomass in artificial urine, while ure- biofilms did not produce biomineral deposits under identical growth conditions. Following exposure to ciprofloxacin, ure+ biofilms showed greater survival (less killing) than ure- biofilms, indicating that biomineralization protected biofilm-resident cells against the antimicrobial. To evaluate the mechanism responsible for this recalcitrance, we observed and quantified the transport of Cy5-conjugated ciprofloxacin into the biofilm by video confocal microscopy. These observations revealed that the reduced susceptibility of ure+ biofilms resulted from hindered delivery of ciprofloxacin into biomineralized regions of the biofilm. Further, biomineralization enhanced retention of viable cells on the surface following antimicrobial exposure. These findings together show that ureolytic biomineralization induced by P. mirabilis metabolism strongly regulates antimicrobial susceptibility by reducing internal solute transport and increasing biofilm stability.
由产脲酶细菌,特别是奇异变形杆菌诱导的尿素分解生物矿化作用,是导致尿路结石形成和留置导尿管结壳的原因。这类微生物生物膜难以根除,并导致与导尿管相关的尿路感染持续存在,但其顽固难除的机制仍不清楚。在本研究中,我们对野生型(ure+)和脲酶阴性(ure-)奇异变形杆菌生物膜对环丙沙星杀灭作用的敏感性进行了表征。在人工尿液中,ure+生物膜产生了细小的生物矿沉淀,这些沉淀均匀分布在生物膜生物质中,而ure-生物膜在相同生长条件下未产生生物矿沉积。暴露于环丙沙星后,ure+生物膜比ure-生物膜表现出更高的存活率(杀灭率更低),这表明生物矿化作用保护了生物膜内的细胞免受抗菌药物的影响。为了评估这种顽固难除的机制,我们通过视频共聚焦显微镜观察并量化了Cy5标记的环丙沙星向生物膜内的转运。这些观察结果表明,ure+生物膜敏感性降低是由于环丙沙星向生物膜矿化区域的递送受阻所致。此外,生物矿化作用增强了抗菌药物暴露后活细胞在表面的保留。这些发现共同表明,奇异变形杆菌代谢诱导的尿素分解生物矿化作用通过减少内部溶质转运和增加生物膜稳定性,强烈调节抗菌药物敏感性。