碱性磷酸酶 LapA 在磷饥饿胁迫下调控 PAO1 群体感应介导的毒力和生物膜形成。
Alkaline phosphatase LapA regulates quorum sensing-mediated virulence and biofilm formation in PAO1 under phosphate depletion stress.
机构信息
Anhui Provincial Key Laboratory of Molecular Enzymology and Mechanism of Major Diseases, College of Life Sciences, Anhui Normal University , Wuhu, Anhui, China.
School of Food and Biology Engineering, Xuzhou University of Technology , Xuzhou, Jiangsu, China.
出版信息
Microbiol Spectr. 2023 Dec 12;11(6):e0206023. doi: 10.1128/spectrum.02060-23. Epub 2023 Oct 5.
Our previous study demonstrated that the expression of lapA was induced under phosphate depletion conditions, but its roles in virulence and biofilm formation by remain largely unknown. This study presents a systematic investigation of the roles of lapA in virulence induction and biofilm formation by constructing a lapA-deficient strain with PAO1. The results showed that deletion of the lapA gene evidently reduced elastase activity, swimming motility, C4-HSL, and 3-oxo-C12-HSL production, and increased rhamnolipid production under phosphate depletion stress. Moreover, lapA gene deletion inhibited PAO1 biofilm formation in porcine skin explants by reducing the expression levels of las and rhl quorum sensing systems and extracellular polymeric substance synthesis. Finally, lapA gene deletion also reduced the virulence of PAO1 in in fast-kill and slow-kill infection assays. This study provides insights into the roles of lapA in modulating virulence and biofilm formation under phosphate depletion stress.
我们之前的研究表明，lapA 的表达在磷酸盐饥饿条件下被诱导，但它在 中的毒力和生物膜形成中的作用在很大程度上仍是未知的。本研究通过构建 lapA 缺失的 PAO1 菌株，对 lapA 在毒力诱导和生物膜形成中的作用进行了系统研究。结果表明，缺失 lapA 基因显著降低了弹性蛋白酶活性、泳动性、C4-HSL 和 3-oxo-C12-HSL 的产生，并增加了在磷酸盐饥饿应激下鼠李糖脂的产生。此外，lapA 基因缺失通过降低 las 和 rhl 群体感应系统以及胞外聚合物合成的表达水平，抑制了 PAO1 在猪皮外植体中的生物膜形成。最后，lapA 基因缺失也降低了 PAO1 在快速杀伤和缓慢杀伤感染模型中的毒力。本研究深入了解了 lapA 在调节 在磷酸盐饥饿应激下的毒力和生物膜形成中的作用。
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