ArticleInfection and immunity2011
Contribution of lethal toxin and edema toxin to the pathogenesis of anthrax meningitis.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Risk Factors for Death or Meningitis in Adults Hospitalized for Cutaneous Anthrax, 1950-2018: A Systematic Review.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2022Pooled it
- Anthrax ET activates Rac1 and RTK signaling to induce F-actin reorganization and endothelial permeability.iScience · 2025Article
- Comprehensive characterization of toxins during progression of inhalation anthrax in a non-human primate model.PLoS pathogens · 2022Article
- Anthrax toxins regulate pain signaling and can deliver molecular cargoes into ANTXR2Nature neuroscience · 2022Article
- Clindamycin Protects Nonhuman Primates Against Inhalational Anthrax But Does Not Enhance Reduction of Circulating Toxin Levels When Combined With Ciprofloxacin.The Journal of infectious diseases · 2021Article
- 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
- Pathology of wild-type and toxin-independent Bacillus anthracis meningitis in rabbits.PloS one · 2017Article
- Diminished but Not Abolished Effect of Two His351 Mutants of Anthrax Edema Factor in a Murine Model.Toxins · 2016Article
- Streptococcus pneumoniae induces pyroptosis through the regulation of autophagy in murine microglia.Oncotarget · 2015Article
- Raxibacumab augments hemodynamic support and improves outcomes during shock with B. anthracis edema toxin alone or together with lethal toxin in canines.Intensive care medicine experimental · 2015Article
- The role of autophagy during group B Streptococcus infection of blood-brain barrier endothelium.The Journal of biological chemistry · 2014Article
- Lethal factor, but not edema factor, is required to cause fatal anthrax in cynomolgus macaques after pulmonary spore challenge.The American journal of pathology · 2014Article
- Impaired colonic B-cell responses by gastrointestinal Bacillus anthracis infection.The Journal of infectious diseases · 2014Article
- Inflammasomes in the CNS.Nature reviews. Neuroscience · 2014Review
- Colonic immune suppression, barrier dysfunction, and dysbiosis by gastrointestinal bacillus anthracis Infection.PloS one · 2014Article
- B. anthracis associated cardiovascular dysfunction and shock: the potential contribution of both non-toxin and toxin components.BMC medicine · 2013Review
- Cholera toxin disrupts barrier function by inhibiting exocyst-mediated trafficking of host proteins to intestinal cell junctions.Cell host & microbe · 2013Article
- B. anthracis edema toxin increases cAMP levels and inhibits phenylephrine-stimulated contraction in a rat aortic ring model.American journal of physiology. Heart and circulatory physiology · 2013Article
- Vector-mediated selective expression of lethal factor, a toxic element of Bacillus anthracis, damages A549 cells via inhibition of MAPK and AKT pathways.International journal of medical sciences · 2013Article
- Anthrax lethal toxin downregulates claudin-5 expression in human endothelial tight junctions.PloS one · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Bacillus anthracis is a Gram-positive spore-forming bacterium that causes anthrax disease in humans and animals. Systemic infection is characterized by septicemia, toxemia, and meningitis, the main neurological complication associated with high mortality. We have shown previously that B. anthracis Sterne is capable of blood-brain barrier (BBB) penetration, establishing the classic signs of meningitis, and that infection is dependent on the expression of both major anthrax toxins, lethal toxin (LT) and edema toxin (ET). Here we further investigate the contribution of the individual toxins to BBB disruption using isogenic toxin mutants deficient in lethal factor, ΔLF, and edema factor, ΔEF. Acute infection with B. anthracis Sterne and the ΔLF mutant resulted in disruption of human brain microvascular endothelial cell (hBMEC) monolayer integrity and tight junction protein zona occludens-1, while the result for cells infected with the ΔEF mutant was similar to that for the noninfected control. A significant decrease in bacterial invasion of BBB endothelium in vitro was observed during infection with the ΔLF strain, suggesting a prominent role for LT in promoting BBB interaction. Further, treatment of hBMECs with purified LT or chemicals that mimic LT action on host signaling pathways rescued the hypoinvasive phenotype of the ΔLF mutant and resulted in increased bacterial uptake. We also observed that toxin expression reduced bacterial intracellular survival by inducing the bulk degradative autophagy pathway in host cells. Finally, in a murine model of anthrax meningitis, mice infected with the ΔLF mutant exhibited no mortality, brain bacterial load, or evidence of meningitis compared to mice infected with the parental or ΔEF strains.
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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.