ArticleBrazilian journal of microbiology : [publication of the Brazilian Society for Microbiology]
The virulence of Streptococcus pneumoniae partially depends on dprA.
Article in Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology]. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Pneumolysin as a target for new therapies against pneumococcal infections: A systematic review.PloS one · 2023Pooled it
- A comparison of routine blood culture methods and multiplex quantitative PCR for detecting pathogens in simulated polymicrobial blood cultures.Journal of medical microbiology · 2026Article
- Genomic and functional dissection of natural transformation-related genes inMicrobiology spectrum · 2026Article
- Allele-specific collateral and fitness effects determine the dynamics of fluoroquinolone resistance evolution.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- DprA-Dependent Exit from the Competent State Regulates Multifaceted Streptococcus pneumoniae Virulence.Infection and immunity · 2019Article
- A Novel Iron Transporter SPD_1590 inFrontiers in microbiology · 2018Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Streptococcus pneumoniae is one of the most frequent opportunistic pathogens worldwide. DNA processing protein A (DprA) is an important factor involved in bacterial uptake and DNA integration into bacterial genome, but its role in S. pneumoniae virulence remains unclear. The aim of this study was to characterize the effects of the pneumococcal dprA gene on the pathogenesis of S. pneumoniae. To construct a dprA-deficient pneumococcal strain, the dprA gene of the S. pneumoniae strain D39 was inactivated. The virulence of this dprA-deficient strain, designated ΔD39, was compared with that of the wild-type strain by evaluating their respective capabilities to adhere to human pulmonary epithelial cells (PEC-A549) and by analyzing their choline-binding protein expression levels. In addition, the expression profiles of genes associated with virulence and host survival assays were also conducted with the mutant and the wild-type strain. Our results indicate that the capability of ΔD39 to adhere to the PEC-A549 airway cells was significantly lower (p<0.01) compared with D39. Additionally, the 100-KD choline-binding protein was not detected in ΔD39. The addition of competence-stimulating peptide (CSP) lead to a significantly reduction of psaA mRNA expression in the dprA-deficient mutant and an increased level of psaA transcripts in the wild-type strain (p<0.01). The median survival time of mice intraperitoneally infected with ΔD39 was significantly higher (p<0.01) than that of mice infected with D39. The results of this study suggest that DprA has a significant effect on virulence characteristics of S. pneumoniae by influencing the expression of choline-binding protein and PsaA.
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