ArticleMolecular microbiology2010
Regulation of CovR expression in Group B Streptococcus impacts blood-brain barrier penetration.
Article in Molecular microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
76 citing papers in PubMed, 107 citations in OpenAlex.
- The diabetic wound microenvironment drives emergence and maintenance of CovRS variants in group BInfection and immunity · 2026Article
- CRISPR interference in aJournal of bacteriology · 2026Article
- Group B streptococcal infections in pregnancy and early life.Clinical microbiology reviews · 2025Review
- Mechanisms and Manifestations of Group B Streptococcus Meningitis in Newborns.Journal of the Pediatric Infectious Diseases Society · 2025Review
- Analysis of serotype distribution and characteristics of nonhemolytic and nonpigmented strains among group B Streptococcus isolates in a southern Taiwan local hospital.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025Article
- 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
- Hyperphosphorylation of the Group A Streptococcal Control of Virulence Regulator Increases Promoter Occupancy Specifically at Virulence Factor-Encoding Genes.Journal of bacteriology · 2023Article
- Group B Streptococcus Cas9 variants provide insight into programmable gene repression and CRISPR-Cas transcriptional effects.Communications biology · 2023Article
- Blood-Brain Barrier Integrity Damage in Bacterial Meningitis: The Underlying Link, Mechanisms, and Therapeutic Targets.International journal of molecular sciences · 2023Review
- In Vivo Role of Two-Component Regulatory Systems in Models of Urinary Tract Infections.Pathogens (Basel, Switzerland) · 2023Review
- Group BScience advances · 2022Article
- Regulatory cross-talk supports resistance to Zn intoxication in Streptococcus.PLoS pathogens · 2022Article
- Group B Streptococcal Neonatal Meningitis.Clinical microbiology reviews · 2022Review
- Genome-Wide CRISPR-Cas9 Screen Does Not Identify Host Factors Modulating Streptococcus agalactiae β-Hemolysin/Cytolysin-Induced Cell Death.Microbiology spectrum · 2022Article
- Article
- CRISPR-dependent endogenous gene regulation is required for virulence in piscineEmerging microbes & infections · 2021Article
- The CovR regulatory network drives the evolution of Group B Streptococcus virulence.PLoS genetics · 2021Article
- Article
- Hemolytic Membrane Vesicles of Group B Streptococcus Promote Infection.The Journal of infectious diseases · 2021Article
- Bacterial and Host Determinants of Group B Streptococcal Vaginal Colonization and Ascending Infection in Pregnancy.Frontiers in cellular and infection microbiology · 2021Review
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Group B Streptococcus (GBS) is an important cause of invasive infections in humans. The pathogen encodes a number of virulence factors including the pluripotent beta-haemolysin/cytolysin (beta-H/C). As GBS has the disposition of both a commensal organism and an invasive pathogen, it is important for the organism to appropriately regulate beta-H/C and other virulence factors in response to the environment. GBS can repress transcription of beta-H/C using the two-component system, CovR/CovS. Recently, we described that the serine/threonine kinase Stk1 can phosphorylate CovR at threonine 65 to relieve repression of beta-H/C. In this study, we show that infection with CovR-deficient GBS strains resulted in increased sepsis. Although CovR-deficient GBS showed decreased ability to invade the brain endothelium in vitro, they were more proficient in induction of permeability and pro-inflammatory signalling pathways in brain endothelium and penetration of the blood-brain barrier (BBB) in vivo. Microarray analysis revealed that CovR positively regulates its own expression and regulates the expression of 153 genes. Collectively, our results suggest that the positive feedback loop which regulates CovR transcription modulates host cell interaction and immune defence and may facilitate the transition of GBS from a commensal organism to a virulent meningeal pathogen.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.