The Role of the Two-Component QseBC Signaling System in Biofilm Formation and Virulence of Hypervirulent Klebsiella pneumoniae ATCC43816.
The Role of the Two-Component QseBC Signaling System in Biofilm Formation and Virulence of Hypervirulent Klebsiella pneumoniae ATCC43816.
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双组分QseBC信号系统在高毒力肺炎克雷伯菌ATCC 43816生物膜形成和毒力中的作用
DOI：
10.3389/fmicb.2022.817494
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发表时间：
2022
影响因子：
5.2
通讯作者：
Du, Hong
中科院分区：
文献类型：
--
作者：
Lv, Jingnan;Zhu, Jie;Wang, Ting;Xie, Xiaofang;Wang, Tao;Zhu, Zhichen;Chen, Liang;Zhong, Fengyun;Du, Hong
高毒力肺炎克雷伯氏菌（hvKP）是一种不断发展的感染性病原体，与高死亡率相关。克雷伯菌的高毒力和多药耐药的融合进一步挑战了临床治疗方案。肺炎感染。QseBC双组分系统（TCS）是群体感应调节级联的组分，并且在大肠杆菌中作为生物膜生长、细菌运动性和毒力的全局调节器起作用。然而，QseBC在hvKP中的功能机制尚未报道，我们的目的是研究QseBC在调节hvKP菌株ATCC 43816中的毒力中的作用。CRISPR-Cas9系统用于在ATCC 43816中构建qseB、qseC和qseBC敲除。在野生型和突变体之间没有检测到生长和抗生素敏感性的显著改变。qseC的缺失导致G. Mellonella模型。RNAseq差异基因表达分析显示，与野生型对照相比，与基因相关的生物膜形成（glgC、glgP、glgA、gcvA、bcsA、ydaM、paaF、ptsG）、细菌VI型分泌系统（virB 4、virB 6、virB 10、vgrG、hcp）和铁载体生物合成（entC、entD、entE）显著上调。此外，qseB、ygiW（编码OB家族蛋白）和AraC家族转录调节因子IT767_23090基因在不存在QseC的情况下表现出最高表达，这可能与毒性增加有关。该研究为QseBC在调节hvKP毒力方面的功能重要性提供了新的见解。
Hypervirulent Klebsiella pneumoniae (hvKP) is an evolving infectious pathogen associated with high mortality. The convergence of hypervirulence and multidrug resistance further challenges the clinical treatment options for K. pneumoniae infections. The QseBC two-component system (TCS) is a component of quorum-sensing regulatory cascade and functions as a global regulator of biofilm growth, bacterial motility, and virulence in Escherichia coli. However, the functional mechanisms of QseBC in hvKP have not been reported, and we aim to examine the role of QseBC in regulating virulence in hvKP strain ATCC43816. The CRISPR-Cas9 system was used to construct qseB, qseC, and qseBC knockout in ATCC43816. No significant alterations in the growth and antibiotic susceptibility were detected between wild-type and mutants. The deletion of qseC led to an increase of biofilm formation, resistance to serum killing, and high mortality in the G. mellonella model. RNAseq differential gene expression analysis exhibited that gene-associated biofilm formation (glgC, glgP, glgA, gcvA, bcsA, ydaM, paaF, ptsG), bacterial type VI secretion system (virB4, virB6, virB10, vgrG, hcp), and biosynthesis of siderophore (entC, entD, entE) were significantly upregulated in comparison with the wild-type control. In addition, qseB, ygiW (encode OB-family protein), and AraC family transcriptional regulator IT767_23090 genes showed highest expressions in the absence of QseC, which might be related to increased virulence. The study provided new insights into the functional importance of QseBC in regulating the virulence of hvKP.
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