QseB mediates biofilm formation and invasion in Salmonella enterica serovar Typhi
QseB mediates biofilm formation and invasion in Salmonella enterica serovar Typhi
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QseB 介导伤寒沙门氏菌生物膜形成和侵袭
DOI：
10.1016/j.micpath.2017.01.010
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发表时间：
2017-03-01
影响因子：
3.8
通讯作者：
Ni, Bin
中科院分区：
文献类型：
--
作者：
Ji, Ying;Li, Wenliang;Ni, Bin
QseB 是 QseBC 双组分系统 (TCS) 的响应调节因子，该系统与群体感应相关，并作为鞭毛、生物膜形成和毒力的全局调节因子。 QseB 的功能及其与 QseC 的相互作用一直是某些生物体中研究的主题，然而，在肠伤寒沙门氏菌（S. Typhi）中所做的工作却很少。本研究的目的是研究 QseB 对伤寒沙门氏菌生物膜形成和毒力的影响。结果表明，与野生型菌株相比，qseC突变体的生物膜形成能力有限。我们还表明 qseB 在 qseC 突变体中过度表达。有趣的是，qseC 突变体中 qseB 的缺失恢复了野生型表型。这些结果表明，QseB 可能是在缺乏 QseC 的情况下生物膜形成受损的原因。此外，野生型细胞中qseB的缺失减少了生物膜的形成，而野生型细胞中qseB的过度表达则增加了生物膜的形成。实时定量 PCR 还揭示了 qseB 过表达菌株中一些菌毛相关基因的上调。这些结果表明，在 QseC 存在的情况下，QseB 可能会增强生物膜的形成。综上所述，我们假设 QseB 具有双重调节功能，这些功能取决于其同源传感器。此外，与野生型相比，qseB 突变体对 HeLa 细胞的侵袭增强，但 qseC 突变体对 HeLa 细胞的侵袭减弱。 invF::lacZ 的 β-半乳糖苷酶活性在 qseB 突变体中增加，但在 qseC 突变体中降低，这与入侵结果一致。总之，QseB 可能对生物膜形成具有双重调节功能，并对伤寒沙门氏菌的毒力起负面作用。 (C) 2017 Elsevier Ltd. 保留所有权利。
QseB is a response regulator of the QseBC two-component system (TCS) which is associated with quorum sensing and functions as a global regulator of flagella, biofilm formation, and virulence. The function of QseB and its interaction with QseC has been the subject of study in some organisms, however, little work was done in Salmonella enterica serovar Typhi (S. Typhi). The objective of this study was to investigate the effect of QseB on biofilm formation and virulence in S. Typhi. It showed that the biofilm formation ability of qseC mutant was limited as compared to the wild type strain. We also show overexpression of qseB was in a qseC mutant. Interestingly, deletion of qseB in a qseC mutant restored a wild type phenotype. These results suggested that QseB may account for the impaired biofilm formation in the absence of QseC. Furthermore, deletion of qseB in wild type cells decreased biofilm formation, whereas over expression of qseB in wild type cells increased biofilm formation. Quantitative real-time PCR also revealed the up-regulation of some fimbria-associated genes in a qseB overexpression strain. These results indicate that QseB may enhance biofilm formation in the presence of QseC. Taken together, we hypothesize that QseB has dual regulatory functions which are dependent upon its cognate sensor. Additionally, invasion of HeLa cells was enhanced in qseB mutant but attenuated in a qseC mutant compared with wild-type. The beta-galactosidase activity of invF::lacZ was increased in qseB mutant but decreased in qseC mutant which was consistent with invasion results. In conclusion, QseB may have dual regulatory functions concerning biofilm formation and plays a negative role in virulence of S. Typhi. (C) 2017 Elsevier Ltd. All rights reserved.