ArticleJournal of bacteriology2012
Regulation and function of pilus island 1 in group B streptococcus.
Article in Journal of bacteriology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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
26 citing papers in PubMed, 46 citations in OpenAlex.
- The response regulator FpsR controls the flagella-pili transition and mucosal colonization inGut microbes · 2025Article
- Group B streptococcal infections in pregnancy and early life.Clinical microbiology reviews · 2025Review
- A Comparative Analysis of Molecular Epidemiology and Antibiotic Resistance in Group B Streptococcus Isolated From Invasive and Noninvasive Adult Cases in Daejeon, South Korea.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2025Article
- Re-framing the importance of Group BInfection and immunity · 2024Review
- T3SS protein EsrC binds to theApplied and environmental microbiology · 2024Article
- Tipping the balance in autoimmunity: are regulatory t cells the cause, the cure, or both?Molecular and cellular pediatrics · 2024Review
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- Macrophage polarization duringFrontiers in microbiology · 2023Article
- A Novel Conserved Protein in Streptococcus agalactiae, BvaP, Is Important for Vaginal Colonization and Biofilm Formation.mSphere · 2022Article
- Serotype Distribution, Virulence Determinants and Antimicrobial Susceptibility of Streptococcus agalactiae Isolated from Young InfantsPathogens (Basel, Switzerland) · 2022Article
- Article
- The CovR regulatory network drives the evolution of Group B Streptococcus virulence.PLoS genetics · 2021Article
- Emerging Fatal Ib/CC12 Hypervirulent MultiresistantFrontiers in microbiology · 2021Article
- The Pathogenic Factors from Oral Streptococci for Systemic Diseases.International journal of molecular sciences · 2019Review
- The Double Life of Group B Streptococcus: Asymptomatic Colonizer and Potent Pathogen.Journal of molecular biology · 2019Review
- Group B Streptococcal Colonization, Molecular Characteristics, and Epidemiology.Frontiers in microbiology · 2018Review
- Contribution of pilus type 2b to invasive disease caused by a Streptococcus agalactiae ST-17 strain.BMC microbiology · 2017Article
- Regulation of PI-2b Pilus Expression in Hypervirulent Streptococcus agalactiae ST-17 BM110.PloS one · 2017Article
- Pilus distribution among lineages of group b streptococcus: an evolutionary and clinical perspective.BMC microbiology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Group B streptococcus (GBS) pili may enhance colonization and infection by mediating bacterial adhesion to host cells, invasion across endothelial and epithelial barriers, and resistance to bacterial ingestion and killing by host phagocytes. However, it remains unclear how pilus expression is regulated and how modulation of pilus production affects GBS interactions with the human host. We investigated the regulation and function of pilus island 1 (PI-1) pili in GBS strain 2603. We found that PI-1 gene expression was controlled by the CsrRS two-component system, by Ape1, an AraC-type regulator encoded by a divergently transcribed gene immediately upstream of PI-1, and by environmental pH. The response regulator CsrR repressed expression of Ape1, which is an activator of PI-1 gene expression. In addition, CsrR repressed PI-1 gene expression directly, independent of its regulation of Ape1. In vitro assays demonstrated specific binding of both CsrR and Ape1 to chromosomal DNA sequences upstream of PI-1. Pilus gene expression was activated by acidic pH, and this effect was independent of CsrRS and Ape1. Unexpectedly, characterization of PI-1 deletion mutants revealed that PI-1 pili do not mediate adhesion of strain 2603 to A549 respiratory epithelial cells, ME180 cervical cells, or VK2 vaginal cells in vitro. PI-1 pili reduced internalization and intracellular killing of GBS by human monocyte-derived macrophages, by approximately 50%, but did not influence complement-mediated opsonophagocytic killing by human neutrophils. These findings shed new light on the complex nature of pilus regulation and function in modulating GBS interactions with the human host.
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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.