ArticleInfection and immunity2007
Anthrax edema toxin sensitizes DBA/2J mice to lethal toxin.
Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- ERK pathway reactivation prevents anthrax toxin lethality in mice.Nature microbiology · 2025Article
- ATP depletion in anthrax edema toxin pathogenesis.PLoS pathogens · 2025Article
- Rapid Discovery and Characterization of Synthetic Neutralizing Antibodies against Anthrax Edema Toxin.Biochemistry · 2019Article
- In vivo dynamics of active edema and lethal factors during anthrax.Scientific reports · 2016Article
- Bacillus anthracis edema factor substrate specificity: evidence for new modes of action.Toxins · 2012Review
- Anthrax edema toxin impairs clearance in mice.Infection and immunity · 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
- The potential contributions of lethal and edema toxins to the pathogenesis of anthrax associated shock.Toxins · 2011Review
- Glycogen synthase kinase 3 activation is important for anthrax edema toxin-induced dendritic cell maturation and anthrax toxin receptor 2 expression in macrophages.Infection and immunity · 2011Article
- Noninvasive imaging technologies reveal edema toxin as a key virulence factor in anthrax.The American journal of pathology · 2011Article
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- Neutralizing monoclonal antibody to edema toxin and its effect on murine anthrax.Infection and immunity · 2010Article
- Cellular and systemic effects of anthrax lethal toxin and edema toxin.Molecular aspects of medicine · 2009Review
- The adenylyl cyclase activity of anthrax edema factor.Molecular aspects of medicine · 2009Review
- The major neutralizing antibody responses to recombinant anthrax lethal and edema factors are directed to non-cross-reactive epitopes.Infection and immunity · 2009Article
- Structure-activity relationship studies of a novel series of anthrax lethal factor inhibitors.Bioorganic & medicinal chemistry · 2009Article
- Bacillus anthracis edema toxin activates nuclear glycogen synthase kinase 3beta.Infection and immunity · 2008Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Anthrax toxin is made up of three separate protein components: the receptor-binding protective antigen (PA), the adenylyl cyclase edema factor (EF), and the metalloproteinase lethal factor (LF). EF and PA constitute edema toxin (ET), which causes edema when injected subcutaneously. At higher doses, ET causes severe pathologies and death in BALB/cJ mice (A. M. Firoved et al., Am. J. Pathol. 167:1309-1320, 2005). A striking effect of ET at lethal doses is adrenal necrosis. Here we show that low doses of ET (10 microg) that produce no overt signs of illness in mice still cause substantial adrenal lesions. These lesions are not associated with reduced corticosterone production; instead, ET-treated mice have increased corticosterone production. Because the resistance of mice to the other component of anthrax toxin, lethal toxin (LT; LF plus PA), has been shown to be overcome by the perturbation of the endocrine system, we hypothesized that sublethal doses of ET might sensitize LT-resistant DBA/2J mice to LT-mediated lethality. We report that a low dose of ET (5 microg) is sufficient to sensitize DBA/2J mice when given concurrently with LT. Higher doses of ET (e.g., 15 microg) given to male and female DBA/2J mice 18 h prior to LT challenge also sensitize them to LT. This study using highly purified ET and LT demonstrates how the components of anthrax toxin can work together to increase lethality.
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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.