ArticleThe American journal of pathology2005
Anthrax lethal toxin induces endothelial barrier dysfunction.
Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 150 citations in OpenAlex.
- Anthrax toxins exacerbate sepsis-induced coagulopathy and endothelial dysfunction in a baboon model of anthrax.Journal of thrombosis and haemostasis : JTH · 2026Article
- Article
- Comprehensive characterization of toxins during progression of inhalation anthrax in a non-human primate model.PLoS pathogens · 2022Article
- The effect of Ethanolic extract of Indonesian propolis on endothelial dysfunction and Multi Organ dysfunction syndrome in anthrax animal model.Saudi journal of biological sciences · 2022Article
- Impact of Bacterial Toxins in the Lungs.Toxins · 2020Review
- Very Early Blood Diffusion of the Active Lethal and Edema Factors of Bacillus anthracis After Intranasal Infection.The Journal of infectious diseases · 2020Article
- Article
- 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
- Review
- Shock and lethality with anthrax edema toxin in rats are associated with reduced arterial responsiveness to phenylephrine and are reversed with adefovir.American journal of physiology. Heart and circulatory physiology · 2017Article
- Anthrax immune globulin improves hemodynamics and survival during B. anthracis toxin-induced shock in canines receiving titrated fluid and vasopressor support.Intensive care medicine experimental · 2017Article
- Soluble P-selectin rescues mice from anthrax lethal toxin-induced mortality through PSGL-1 pathway-mediated correction of hemostasis.Virulence · 2017Article
- Article
- Bacteria and endothelial cells: a toxic relationship.Current opinion in microbiology · 2017Review
- Iron and zinc exploitation during bacterial pathogenesis.Metallomics : integrated biometal science · 2015Review
- The Saccharomyces boulardii CNCM I-745 strain shows protective effects against the B. anthracis LT toxin.Toxins · 2015Article
- Review
- Targeted silencing of anthrax toxin receptors protects against anthrax toxins.The Journal of biological chemistry · 2014Article
- Asymmetric dimethylarginine levels in patients with cutaneous anthrax: a laboratory analysis.Annals of clinical microbiology and antimicrobials · 2014Article
- Platelet-activating factor contributes to Bacillus anthracis lethal toxin-associated damage.The Journal of biological chemistry · 2014Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hemorrhage and pleural effusion are prominent pathological features of systemic anthrax infection. We examined the effect of anthrax lethal toxin (LT), a major virulence factor of Bacillus anthracis, on the barrier function of primary human lung microvascular endothelial cells. We also examined the distribution patterns of cytoskeletal actin and vascular endothelial-cadherin (VE-cadherin), both of which are involved in barrier function regulation. Endothelial monolayers cultured on porous membrane inserts were treated with the LT components lethal factor (LF) and protective antigen (PA) individually, or in combination. LT induced a concentration- and time-dependent decrease in transendothelial electrical resistance that correlated with increased permeability to fluorescently labeled albumin. LT also produced a marked increase in central actin stress fibers and significantly altered VE-cadherin distribution as revealed by immunofluorescence microscopy and cell surface enzyme-linked immunosorbent assay. Treatment with LF, PA, or the combination of an inactive LF mutant and PA did not alter barrier function or the distribution of actin or VE-cadherin. LT-induced barrier dysfunction was not dependent on endothelial apoptosis or necrosis. The present findings support a possible role for LT-induced barrier dysfunction in the vascular permeability changes accompanying systemic anthrax infection.
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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.