ArticleJournal of bacteriology2009
Penetration of the blood-brain barrier by Bacillus anthracis requires the pXO1-encoded BslA protein.
Article in Journal of bacteriology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 39 citations in OpenAlex.
- Breaking the fortress: a mechanistic review of meningitis-causing bacteria breaching tactics in blood brain barrier.Cell communication and signaling : CCS · 2025Review
- Pleiotropic functions of CpdB in Bacillus anthracis.World journal of microbiology & biotechnology · 2025Article
- Enrichment of infection-associated bacteria in the low biomass brain bacteriota of Alzheimer's disease patients.PloS one · 2024Article
- Blood-Brain Barrier Integrity Damage in Bacterial Meningitis: The Underlying Link, Mechanisms, and Therapeutic Targets.International journal of molecular sciences · 2023Review
- Alternate atxA and acpA dependent response of Bacillus anthracis to serum, HCO3- and CO2.PloS one · 2023Article
- NLRP6 Serves as a Negative Regulator of Neutrophil Recruitment and Function DuringFrontiers in microbiology · 2022Article
- TheMicroorganisms · 2020Review
- Infection with a NonencapsulatedToxins · 2018Article
- Mechanisms of Blood Brain Barrier Disruption by Different Types of Bacteria, and Bacterial-Host Interactions Facilitate the Bacterial Pathogen Invading the Brain.Cellular and molecular neurobiology · 2018Review
- Assembly and Function of the Bacillus anthracis S-Layer.Annual review of microbiology · 2017Review
- Pathology of wild-type and toxin-independent Bacillus anthracis meningitis in rabbits.PloS one · 2017Article
- Bacillus anthracis S-layer protein BslA binds to extracellular matrix by interacting with laminin.BMC microbiology · 2016Article
- The role of autophagy during group B Streptococcus infection of blood-brain barrier endothelium.The Journal of biological chemistry · 2014Article
- Transcriptome analysis identifies Bacillus anthracis genes that respond to CO2 through an AtxA-dependent mechanism.BMC genomics · 2014Article
- The central nervous system as target of Bacillus anthracis toxin independent virulence in rabbits and guinea pigs.PloS one · 2014Article
- Article
- Defense at the border: the blood-brain barrier versus bacterial foreigners.Future microbiology · 2012Review
- New insights into the biological effects of anthrax toxins: linking cellular to organismal responses.Microbes and infection · 2012Review
- Cellular and physiological effects of anthrax exotoxin and its relevance to disease.Frontiers in cellular and infection microbiology · 2012Review
- Contribution of lethal toxin and edema toxin to the pathogenesis of anthrax meningitis.Infection and immunity · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Anthrax is a zoonotic disease caused by the gram-positive spore-forming bacterium Bacillus anthracis. Human infection occurs after the ingestion, inhalation, or cutaneous inoculation of B. anthracis spores. The subsequent progression of the disease is largely mediated by two native virulence plasmids, pXO1 and pXO2, and is characterized by septicemia, toxemia, and meningitis. In order to produce meningitis, blood-borne bacteria must interact with and breach the blood-brain barrier (BBB) that is composed of a specialized layer of brain microvascular endothelial cells (BMEC). We have recently shown that B. anthracis Sterne is capable of penetrating the BBB in vitro and in vivo, establishing the classic signs of meningitis; however, the molecular mechanisms underlying the central nervous system (CNS) tropism are not known. Here, we show that attachment to and invasion of human BMEC by B. anthracis Sterne is mediated by the pXO1 plasmid and an encoded envelope factor, BslA. The results of studies using complementation analysis, recombinant BslA protein, and heterologous expression demonstrate that BslA is both necessary and sufficient to promote adherence to brain endothelium. Furthermore, mice injected with the BslA-deficient strain exhibited a significant decrease in the frequency of brain infection compared to mice injected with the parental strain. In addition, BslA contributed to BBB breakdown by disrupting tight junction protein ZO-1. Our results identify the pXO1-encoded BslA adhesin as a critical mediator of CNS entry and offer new insights into the pathogenesis of anthrax meningitis.
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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.