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Published on: February 23, 2014
SPD_0090 Negatively Contributes to Virulence of Streptococcus pneumoniae
Linlin Cao1, Nan Li1, Yingshan Dong1
1MOE Key Laboratory of Tumor Molecular Biology and Key Laboratory of Functional Protein Research of Guangdong Higher Education Institutes, Institute of Life and Health Engineering, College of Life Science and Technology, Jinan University, Guangzhou, China.
Abstract:
In most bacteria, iron plays an important role in the survival of bacteria and the process of infection to the host. Streptococcus pneumoniae (S. pneumoniae) evolved three iron transporters (i.e., PiaABC, PiuABC, and PitABC) responsible for the transportation of three kinds of iron (i.e., ferrichrome, hemin, and ferric ion). Our previous study showed that both mRNA and protein levels of SPD_0090 were significantly upregulated in the ΔpiuA/ΔpiaA/ΔpitA triple mutant, but its detailed biological function is unknown. In this study, we constructed spd_0090 knockout and complement strain and found that the deletion of spd_0090 hinders bacterial growth. SPD_0090 is located on the cell membrane and affects the hemin utilization ability of S. pneumoniae. The cell infection model showed that the knockout strain had stronger invasion and adhesion ability. Notably, knockout of the spd_0090 gene resulted in an enhanced infection ability of S. pneumoniae in mice by increasing the expression of virulence factors. Furthermore, iTRAQ quantitative proteomics studies showed that the knockout of spd_0090 inhibited carbon metabolism and thus suppressed bacterial growth. Our study showed that SPD_0090 negatively regulates the virulence of S. pneumoniae.
Insights
SPD_0090 negatively regulates the virulence of Streptococcus pneumoniae (S. pneumoniae). Deleting SPD_0090 hinders bacterial growth but enhances S. pneumoniae infection in mice by increasing virulence factors.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Molecular Biology
Background:
- Iron is crucial for bacterial survival and host infection.
- Streptococcus pneumoniae utilizes iron via PiaABC, PiuABC, and PitABC transporters.
- The function of SPD_0090 in S. pneumoniae remained largely unknown despite its upregulation in iron transporter mutants.
Purpose of the Study:
- To elucidate the biological function of SPD_0090 in Streptococcus pneumoniae.
- To investigate the role of SPD_0090 in bacterial growth, iron utilization, and virulence.
- To understand the impact of SPD_0090 on host-pathogen interactions.
Main Methods:
- Construction and analysis of spd_0090 knockout and complement strains.
- Assessment of bacterial growth and hemin utilization.
- Evaluation of invasion, adhesion, and infection capabilities in cell and mouse models.
- iTRAQ quantitative proteomics to analyze metabolic changes.
Main Results:
- SPD_0090 deletion hinders bacterial growth and affects hemin utilization.
- The spd_0090 knockout strain exhibited enhanced invasion, adhesion, and infection in mice.
- Knockout of spd_0090 increased the expression of virulence factors and inhibited carbon metabolism.
- SPD_0090 is a cell membrane protein involved in regulating S. pneumoniae virulence.
Conclusions:
- SPD_0090 negatively regulates the virulence of Streptococcus pneumoniae.
- The absence of SPD_0090 leads to altered metabolism and increased pathogenicity.
- SPD_0090 represents a potential target for controlling S. pneumoniae infections.
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