Dataset Information

The impact of sseK2 deletion on Salmonella enterica serovar typhimurium virulence in vivo and in vitro.

ABSTRACT:

Background

Salmonella enterica is regarded as a major public health threat worldwide. Salmonella secretes the novel translocated effector protein K2 (SseK2), but it is unclear whether this protein plays a significant role in Salmonella enterica Typhimurium virulence.

Results

A ?sseK2 mutant of S. Typhimurium exhibited similar growth curves, adhesion and invasive ability compared with wild-type (WT) bacteria. However, deletion of sseK2 rendered Salmonella deficient in biofilm formation and the early proliferative capacity of the ?sseK2 mutant was significantly lower than that of the WT strain. In vivo, the LD₅₀ (median lethal dose) of the ?sseK2 mutant strain was increased 1.62?×?10³-fold compared with the WT strain. In addition, vaccinating mice with the ?sseK2 mutant protected them against challenge with a lethal dose of the WT strain. The ability of the ?sseK2 mutant strain to induce systemic infection was highly attenuated compared with the WT strain, and the bacterial load in the animals' internal organs was lower when they were infected with the ?sseK2 mutant strain than when they were infected with the WT strain.

Conclusions

We conclude that sseK2 is a virulence-associated gene that plays a vital role in Salmonella virulence.

SUBMITTER: Zhang X

PROVIDER: S-EPMC6686396 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature

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Publications

The impact of sseK2 deletion on Salmonella enterica serovar typhimurium virulence in vivo and in vitro.

Zhang Xiaojie X He Lei L Zhang Chunjie C Yu Chuan C Yang Yadong Y Jia Yanyan Y Cheng Xiangchao X Li Yinju Y Liao Chengshui C Li Jing J Yu Zuhua Z Du Fuyu F

BMC microbiology 20190807 1

<h4>Background</h4>Salmonella enterica is regarded as a major public health threat worldwide. Salmonella secretes the novel translocated effector protein K2 (SseK2), but it is unclear whether this protein plays a significant role in Salmonella enterica Typhimurium virulence.<h4>Results</h4>A ΔsseK2 mutant of S. Typhimurium exhibited similar growth curves, adhesion and invasive ability compared with wild-type (WT) bacteria. However, deletion of sseK2 rendered Salmonella deficient in biofilm forma ...[more]

PMID: 31390974

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Project description:To cause a systemic infection, Salmonella must respond to many environmental cues during mouse infection and express specific subsets of genes in a temporal and spatial manner, but the regulatory pathways are poorly established. To unravel how micro-environmental signals are processed and integrated into coordinated action, we constructed in-frame non-polar deletions of 83 regulators inferred to play a role in Salmonella enteriditis Typhimurium (STM) virulence and tested them in three virulence assays (intraperitoneal [i.p.], and intragastric [i.g.] infection in BALB/c mice, and persistence in 129X1/SvJ mice). Overall, 35 regulators were identified whose absence attenuated virulence in at least one assay, and of those, 14 regulators were required for systemic mouse infection, the most stringent virulence assay. As a first step towards understanding the interplay between a pathogen and its host from a systems biology standpoint, we focused on these 14 genes. Transcriptional profiles were obtained for deletions of each of these 14 regulators grown under four different environmental conditions. These results, as well as publicly available transcriptional profiles, were analyzed using both network inference and cluster analysis algorithms. The analysis predicts a regulatory network in which all 14 regulators control the same set of genes necessary for Salmonella to cause systemic infection. We tested the regulatory model by expressing a subset of the regulators in trans and monitoring transcription of 7 known virulence factors located within Salmonella pathogenicity island 2 (SPI-2). These experiments validated the regulatory model and showed that the response regulator SsrB and the MarR type regulator, SlyA, are the terminal regulators in a cascade that integrates multiple signals. Furthermore, experiments to demonstrate epistatic relationships showed that SsrB can replace SlyA and, in some cases, SlyA can replace SsrB for expression of SPI-2 encoded virulence factors.

Dataset Information

The impact of sseK2 deletion on Salmonella enterica serovar typhimurium virulence in vivo and in vitro.

Background

Results

Conclusions

Publications

The impact of sseK2 deletion on Salmonella enterica serovar typhimurium virulence in vivo and in vitro.

Similar Datasets

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