ArticleNature communications2011
Bacterial Pili exploit integrin machinery to promote immune activation and efficient blood-brain barrier penetration.
Article in Nature communications, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
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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.
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Who cites it
94 citing papers in PubMed, 143 citations in OpenAlex.
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- 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
- Infection of endothelial cells by Streptococcus agalactiae reveals potential role of PI-2b pilus on endothelial barrier dysfunction.Memorias do Instituto Oswaldo Cruz · 2025Article
- Molecular mechanisms of streptococcal disruption of the blood-brain barrier and their pathogenic role in bacterial meningitis.Frontiers in immunology · 2025Review
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- Identification of Glyoxalase A in Group BbioRxiv : the preprint server for biology · 2024Article
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- CsiR-Mediated Signal Transduction Pathway in Response to Low Iron Conditions Promotes Escherichia coli K1 Invasion and Penetration of the Blood-Brain Barrier.The Journal of infectious diseases · 2024Article
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- Stimulation of tumoricidal immunity via bacteriotherapy inhibits glioblastoma relapse.Nature communications · 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
- Occludin and collagen IV degradation mediated by the T9SS effector SspA contributes to blood-brain barrier damage in ducks during Riemerella anatipestifer infection.Veterinary research · 2024Article
- Review
34 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Group B Streptococcus (GBS) is the leading cause of meningitis in newborn infants. Bacterial cell surface appendages, known as pili, have been recently described in streptococcal pathogens, including GBS. The pilus tip adhesin, PilA, contributes to GBS adherence to blood-brain barrier (BBB) endothelium; however, the host receptor and the contribution of PilA in central nervous system (CNS) disease pathogenesis are unknown. Here we show that PilA binds collagen, which promotes GBS interaction with the α₂β₁ integrin resulting in activation of host chemokine expression and neutrophil recruitment during infection. Mice infected with the PilA-deficient mutant exhibit delayed mortality, a decrease in neutrophil infiltration and bacterial CNS dissemination. We find that PilA-mediated virulence is dependent on neutrophil influx as neutrophil depletion results in a decrease in BBB permeability and GBS-BBB penetration. Our results suggest that the bacterial pilus, specifically the PilA adhesin, has a dual role in immune activation and bacterial entry into the CNS.
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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.