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Brucella suis

ABSTRACT: Brucella suis Raw sequence reads

PROVIDER: PRJNA497793 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR8550480_1.fastq.gz	Fastqsanger.gz
	SRR8550480_2.fastq.gz	Fastqsanger.gz
	SRR8550490_1.fastq.gz	Fastqsanger.gz
	SRR8550490_2.fastq.gz	Fastqsanger.gz
	SRR8550500_1.fastq.gz	Fastqsanger.gz

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Integrated proteomic and transcriptomic analyses reveal the roles of Brucella BI-1 in cell division and membrane homeostasis of Brucella suis S2

Project description:To explore the role of Brucella BI-1 in Brucella suis S2, we constructed the Brucella BI-1 deletion mutant strain and its complementary strain. We then determined the effect of Brucella BI-1 deletion on the physiological characteristics of Brucella suis S2 and revealed them via integrated transcriptomic and proteomic analyses. Brucella BI-1 deletion altered the membrane properties of Brucella suis S2 and decreased its resistance to acidic pH, H2O2, polymyxin B, and lincomycin. Additionally, deleting Brucella BI-1 led to defective growth, cell division, and viability in Brucella suis S2. In conclusion, our results revealed that Brucella BI-1 is a bacterial cytoprotective protein involved in membrane homeostasis, cell division, and stress resistance in Brucella suis S2.

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Project description:Neurobrucellosis is a serious complication of brucellosis, which poses a significant threat to human health and quality of life. The origin of this phenomenon is that the patients are more vulnerable to the development of chronic Brucella infection, which is also an important clinical problem. The regulation of Brucella on microglia apoptosis is a primary contributor to chronic neurobrucellosis, nevertheless, the precise molecular mechanism remains incompletely understood. In our research, human microglial clone 3 (HMC3) cells were infected with Brucella suis vaccine strain S2 (B. suis S2) at different MOI for different times to evaluate the influences of B. suis S2 on the IRE1/Caspase-12/Caspase-3 pathway. Subsequently, under the conditions of IRE1/Caspase-12/Caspase-3 pathway was suppressed by B. suis S2, CALR protein was screened by ubiquitin-modified proteomics. Eventually, we infected CALR-overexpression and -knockdown HMC3 cell lines with B. suis S2 to elucidate the molecular mechanism by which the B. suis S2 inhibited HMC3 cells apoptosis. In summary, we confirm that B. suis S2 inhibits apoptosis in HMC3 cells mediated by the IRE1/Caspase-12/Caspase-3 pathway through modulation of CALR ubiquitination. Our study establishes the theoretical foundation for investigating the mechanisms underlying neurobrucellosis and provides a guidance for the clinical treatment of neurobrucellosis.

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