ArticleThe Journal of infectious diseases2017
Effect of the Streptococcus agalactiae Virulence Regulator CovR on the Pathogenesis of Urinary Tract Infection.
Article in The Journal of infectious diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- The diabetic wound microenvironment drives emergence and maintenance of CovRS variants in group BInfection and immunity · 2026Article
- Metagenomic insights into microbial community alterations and co-occurrence networks in infective endocarditis.Genomics & informatics · 2025Article
- Group B streptococcal infections in pregnancy and early life.Clinical microbiology reviews · 2025Review
- Evaluation of Immunostimulatory Effects of Bacterial Lysate Proteins on THP-1 Macrophages: Pro-inflammatory Cytokine Response and Proteomic Profiling.Journal of immunology research · 2025Article
- Endolysin EN572-5 as an alternative to treat urinary tract infection caused by Streptococcus agalactiae.Applied microbiology and biotechnology · 2024Article
- An opportunistic pathogen under stress: how Group B Streptococcus responds to cytotoxic reactive species and conditions of metal ion imbalance to survive.FEMS microbiology reviews · 2024Review
- Alterations in cell arrangements of group B streptococcus due to virulence factor expression can bias estimates of bacterial populations based on colony count measures.Microbiology (Reading, England) · 2024Article
- In Vivo Role of Two-Component Regulatory Systems in Models of Urinary Tract Infections.Pathogens (Basel, Switzerland) · 2023Review
- Variable resistance to zinc intoxication amongFrontiers in immunology · 2023Article
- Group B streptococcus virulence factors associated with different clinical syndromes: Asymptomatic carriage in pregnant women and early-onset disease in the newborn.Frontiers in microbiology · 2023Article
- Regulatory cross-talk supports resistance to Zn intoxication in Streptococcus.PLoS pathogens · 2022Article
- Molecular Characteristic, Antibiotic Resistance, and Detection of Highly Immunoreactive Proteins of Group B Streptococcus Strains Isolated From Urinary Tract Infections in Polish Adults.Frontiers in microbiology · 2022Article
- Article
- CRISPR-dependent endogenous gene regulation is required for virulence in piscineEmerging microbes & infections · 2021Article
- Copper Intoxication in Group B Streptococcus Triggers Transcriptional Activation of theJournal of bacteriology · 2021Article
- Article
- Genetic Basis Underlying the Hyperhemolytic Phenotype of Streptococcus agalactiae Strain CNCTC10/84.Journal of bacteriology · 2020Article
- The Novel Streptococcal Transcriptional Regulator XtgS Negatively Regulates Bacterial Virulence and Directly Represses PseP Transcription.Infection and immunity · 2020Article
- Two-Component Signal Transduction Systems in the Human Pathogen Streptococcus agalactiae.Infection and immunity · 2020Review
- The Fungal PathogenFrontiers in cellular and infection microbiology · 2019Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Streptococcus agalactiae can cause urinary tract infection (UTI). The role of the S. agalactiae global virulence regulator, CovR, in UTI pathogenesis is unknown. Methods: We used murine and human bladder uroepithelial cell models of UTI and S. agalactiae mutants in covR and related factors, including β-hemolysin/cytolysin (β-h/c), surface-anchored adhesin HvgA, and capsule to study the role of CovR in UTI. Results: We found that covR-deficient serotype III S. agalactiae 874391 was significantly attenuated for colonization in mice and adhesion to uroepithelial cells. Mice infected with covR-deficient S. agalactiae produced less proinflammatory cytokines than those infected with wild-type 874391. Acute cytotoxicity in uroepithelial cells triggered by covR-deficient but not wild-type 874391 was associated with significant caspase 3 activation. Mechanistically, covR mutation significantly altered the expression of several genes in S. agalactiae 874391 that encode key virulence factors, including β-h/c and HvgA, but not capsule. Subsequent mutational analyses revealed that HvgA and capsule, but not the β-h/c, exerted significant effects on colonization of the murine urinary tract in vivo. Conclusions: S. agalactiae CovR promotes bladder infection and inflammation, as well as adhesion to and viability of uroepithelial cells. The pathogenesis of S. agalactiae UTI is complex, multifactorial, and influenced by virulence effects of CovR, HvgA, and capsule.
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