ArticleInfection and immunity2006
Anthrax lethal toxin induces ketotifen-sensitive intradermal vascular leakage in certain inbred mice.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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Who cites it
33 citing papers in PubMed, 53 citations in OpenAlex.
- Quantification of immunoglobulin G as an alternative method to the Miles Evans blue assay to measure vascular hyperpermeability induced by infection and sterile inflammation.Biology methods & protocols · 2026Article
- Review
- Breaking the fortress: a mechanistic review of meningitis-causing bacteria breaching tactics in blood brain barrier.Cell communication and signaling : CCS · 2025Review
- 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
- Innate Immune Interactions betweenFrontiers in cellular and infection microbiology · 2018Article
- Review
- A Neutralizing Monoclonal IgG1 Antibody of Platelet-Activating Factor Acetylhydrolase SsE Protects Mice against Lethal Subcutaneous Group A Streptococcus Infection.Infection and immunity · 2015Article
- Bacillus anthracis genomic DNA enhances lethal toxin-induced cytotoxicity through TNF-α production.BMC microbiology · 2014Article
- Molecular determinants for a cardiovascular collapse in anthrax.Frontiers in bioscience (Elite edition) · 2014Review
- 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
- Impaired function of the Tie-2 receptor contributes to vascular leakage and lethality in anthrax.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Protective antigen antibody augments hemodynamic support in anthrax lethal toxin shock in canines.The Journal of infectious diseases · 2012Article
- 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
- Article
- Anthrax infection.American journal of respiratory and critical care medicine · 2011Review
- The potential contributions of lethal and edema toxins to the pathogenesis of anthrax associated shock.Toxins · 2011Review
- Article
- Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Bacillus anthracis lethal toxin (LT) is a bipartite toxin composed of protective antigen (PA) and lethal factor (LF). Injection of LT produces clinical signs characteristic of anthrax infection, including pleural edema and vascular collapse in various animal models. We utilized the classic Miles leakage assay to quantify vascular leakage in mice. LT injected intradermally induced leakage as early as 15 to 25 min in some inbred mouse strains, but not in others, whereas PA or LF individually did not induce leakage. A third component of anthrax toxin, edema factor, did not induce leakage alone or with PA. Leakage was quantified in eight mouse strains, and no correlation was found between sensitivity to intradermal leakage and sensitivity to the lethality of systemically administered LT. The leakage could be inhibited by ketotifen, an inhibitor of mast cell degranulation, but not by azelastine, a histamine receptor 1 antagonist, or by ketanserin, a serotonin 5-HT2A receptor antagonist. LT was cytotoxic to MC/9 mast cells (in vitro) by 7 h after toxin treatment but did not induce histamine release from these cells. Mast cell-deficient mice exhibited the leakage event and had no increased resistance to systemic LT. Human umbilical vein endothelial cells were resistant to LT over 12 h, with only 20% of cells succumbing by 24 h, suggesting that endothelial cell killing is not the cause of the rapid LT-mediated leakage event. We describe here a ketotifen-sensitive vascular leakage event induced by LT which is the most rapid in vivo or in vitro LT-mediated effect reported to date.
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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.