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Complementary Regulation of BfmRS Two-Component and AbaIR Quorum Sensing Systems to Express Virulence-Associated Genes in Acinetobacter baumannii
被引:17
|作者:
Kim, Hyo-Jeong
[1
]
Kim, Na-Yeong
[1
]
Ko, Seo-Yeon
[1
]
Park, Seong-Yong
[1
]
Oh, Man-Hwan
[2
]
Shin, Min-Sang
[1
]
Lee, Yoo-Chul
[1
]
Lee, Je-Chul
[1
]
机构:
[1] Kyungpook Natl Univ, Sch Med, Dept Microbiol, Daegu 41944, South Korea
[2] Dankook Univ, Coll Sci & Technol, Dept Microbiol, Cheonan 16890, South Korea
基金:
新加坡国家研究基金会;
关键词:
Acinetobacter baumannii;
virulence factor;
two-component system;
quorum sensing system;
BfmRS;
RESISTANCE;
D O I:
10.3390/ijms232113136
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Acinetobacter baumannii expresses various virulence factors to adapt to hostile environments and infect susceptible hosts. This study investigated the regulatory network of the BfmRS two-component and AbaIR quorum sensing (QS) systems in the expression of virulence-associated genes in A. baumannii ATCC 17978. The Delta bfmS mutant exhibited a significant decrease in surface motility, which presumably resulted from the low expression of pilT and A1S_0112-A1S_0119 gene cluster. The Delta bfmR mutant displayed a significant reduction in biofilm and pellicle formation due to the low expression of csu operon. The deletion of abaR did not affect the expression of bfmR or bfmS. However, the expression of abaR and abaI was upregulated in the Delta bfmR mutant. The Delta bfmR mutant also produced more autoinducers than did the wild-type strain, suggesting that BfmR negatively regulates the AbaIR QS system. The Delta bfmS mutant exhibited no autoinducer production in the bioassay system. The expression of the A1S_0112-A1S_0119 gene cluster was downregulated in the Delta abaR mutant, whereas the expression of csu operon was upregulated in this mutant with a high cell density. In conclusion, for the first time, we demonstrated that the BfmRS-AbaIR QS system axis regulated the expression of virulence-associated genes in A. baumannii. This study provides new insights into the complex network system involved in the regulation of virulence-associated genes underlying the pathogenicity of A. baumannii.
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