Pleiotropic roles of uvrY on biofilm formation, motility and virulence in uropathogenic Escherichia coli CFT073.

Pleiotropic roles of uvrY on biofilm formation, motility and virulence in uropathogenic Escherichia coli CFT073.
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DOI:
10.1371/journal.pone.0055492
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Mukhopadhyay S
Mukhopadhyay S
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Mitra A;Palaniyandi S;Herren CD;Zhu X;Mukhopadhyay S

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主要由尿路致病性大肠杆菌菌株引起的尿路感染在发达国家和发展中国家仍然是一个重大的公共卫生问题。在泌尿系统发病中,一个重要的毒力决定因素是生物膜的形成,这需要菌毛、鞭毛和其他表面成分(如脂多糖)的表达。在这项研究中,我们探讨了uvrY和csrA基因在尿路致病性大肠杆菌生物膜形成、运动和毒力决定因素中的调控作用。我们发现uvrY突变抑制了聚氯乙烯、聚苯乙烯和玻璃等非生物表面上生物膜的形成,而突变体中uvrY的互补恢复了生物膜的表型。我们进一步评估了uvrY基因在1型菌毛表达中的作用,1型菌毛是一种重要的粘附素,可以促进粘附在各种非生物表面。我们发现,在转录水平上,uvrY调节了1型微纤维在固定模式和固定模式之间的相位变化。缺失突变体极大地降低了毛际重组酶基因的表达,如fimB、fme和fimA,一个编码毛际主要亚基的基因。此外,在缺失突变体中,毒力特异性基因如papA、hlyB和galU的转录也减少了。突变体的群体运动和flhD和flhC的表达也减少。综上所述,我们的发现揭示了uvery促进尿路致病性大肠杆菌生物膜形成、持久性和毒力的可能机制。
Urinary tract infections primarily caused by uropathogenic strains of Escherichia coli (E. coli) remain a significant public health problem in both developed and developing countries. An important virulence determinant in uropathogenesis is biofilm formation which requires expression of fimbriae, flagella, and other surface components such as lipopolysaccharides. In this study, we explored the regulation of uvrY and csrA genes in biofilm formation, motility and virulence determinants in uropathogenic E. coli. We found that mutation in uvrY suppressed biofilm formation on abiotic surfaces such as polyvinyl chloride, polystyrene and glass, and complementation of uvrY in the mutant restored the biofilm phenotype. We further evaluated the role of uvrY gene in expression of type 1 fimbriae, an important adhesin that facilitates adhesion to various abiotic surfaces. We found that phase variation of type 1 fimbriae between fimbriated and afimbriated mode was modulated by uvrY at its transcriptional level. Deletion mutant of uvrY lowered expression of fimbrial recombinase genes, such as fimB, fimE, and fimA, a gene encoding major fimbrial subunit. Furthermore, transcription of virulence specific genes such as papA, hlyB and galU was also reduced in the deletion mutant. Swarming motility and expression of flhD and flhC was also diminished in the mutant. Taken together, our findings unravel a possible mechanism in which uvrY facilitates biofilm formation, persistence and virulence of uropathogenic E. coli.
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