Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, People's Republic of China.
Curr Microbiol. 2023 Mar 6;80(4):126. doi: 10.1007/s00284-023-03226-y.
Hypervirulent Klebsiella pneumoniae (hvKp) strains that form biofilms have recently emerged worldwide; however, the mechanisms underlying biofilm formation and disruption remain elusive. In this study, we established a hvKp biofilm model, investigated its in vitro formation pattern, and determined the mechanism of biofilm destruction by baicalin (BA) and levofloxacin (LEV). Our results revealed that hvKp exhibited a strong biofilm-forming ability, forming early and mature biofilms after 3 and 5 d, respectively. Early biofilm and bacterial burden were significantly reduced by BA + LEV and EM + LEV treatments, which destroyed the 3D structure of early biofilms. Conversely, these treatments were less effective against mature biofilm. The expression of both AcrA and wbbM was significantly downregulated in the BA + LEV group. These findings indicated that BA + LEV might inhibit the formation of hvKp biofilm by altering the expression of genes regulating efflux pumps and lipopolysaccharide biosynthesis.
产超广谱β-内酰胺酶肺炎克雷伯菌(hvKp)生物膜形成株最近在全球范围内出现;然而,生物膜形成和破坏的机制仍不清楚。在本研究中,我们建立了 hvKp 生物膜模型,研究了其体外形成模式,并确定了黄芩苷(BA)和左氧氟沙星(LEV)破坏生物膜的机制。结果表明,hvKp 具有很强的生物膜形成能力,分别在 3 和 5 天后形成早期和成熟生物膜。BA+LEV 和 EM+LEV 处理显著降低了早期生物膜和细菌负荷,破坏了早期生物膜的 3D 结构。然而,这些处理对成熟生物膜的效果较差。BA+LEV 组中 AcrA 和 wbbM 的表达均显著下调。这些发现表明,BA+LEV 可能通过改变调节外排泵和脂多糖生物合成的基因表达来抑制 hvKp 生物膜的形成。