ArticleBiochemical and biophysical research communications2010
The role of anthrolysin O in gut epithelial barrier disruption during Bacillus anthracis infection.
Article in Biochemical and biophysical research communications, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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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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.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- The Biological Role of Conoporins, Actinoporin-like Pore-Forming Toxins from Cone Snails.Toxins · 2025Review
- Early Circulating Edema Factor in Inhalational Anthrax Infection: Does It Matter?Microorganisms · 2024Article
- Some Peculiarities of Anthrax Epidemiology in Herbivorous and Carnivorous Animals.Life (Basel, Switzerland) · 2022Review
- Interaction of Macrophages and Cholesterol-Dependent Cytolysins: The Impact on Immune Response and Cellular Survival.Toxins · 2020Review
- TheMicrobiology spectrum · 2019Review
- Listeriolysin O: A phagosome-specific cytolysin revisited.Cellular microbiology · 2019Review
- Bacterial Virulence Factors: Secreted for Survival.Indian journal of microbiology · 2017Review
- Profiling lethal factor interacting proteins from human stomach using T7 phage display screening.Molecular medicine reports · 2016Article
- New insights into gastrointestinal anthrax infection.Trends in molecular medicine · 2015Review
- Time dynamics of the Bacillus cereus exoproteome are shaped by cellular oxidation.Frontiers in microbiology · 2015Article
- Listeriolysin O Affects the Permeability of Caco-2 Monolayer in a Pore-Dependent and Ca2+-Independent Manner.PloS one · 2015Article
- Crossing of the epithelial barriers by Bacillus anthracis: the Known and the Unknown.Frontiers in microbiology · 2015Review
- Article
- Role of pore-forming toxins in bacterial infectious diseases.Microbiology and molecular biology reviews : MMBR · 2013Review
- Activated protein C ameliorates Bacillus anthracis lethal toxin-induced lethal pathogenesis in rats.Journal of biomedical science · 2012Article
- Expression of TNFAIP3 in intestinal epithelial cells protects from DSS- but not TNBS-induced colitis.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Bacillus anthracis factors for phagosomal escape.Toxins · 2012Review
- Restricting fermentative potential by proteome remodeling: an adaptive strategy evidenced in Bacillus cereus.Molecular & cellular proteomics : MCP · 2012Article
- New insights into the biological effects of anthrax toxins: linking cellular to organismal responses.Microbes and infection · 2012Review
- Anthrolysin O and fermentation products mediate the toxicity of Bacillus anthracis to lung epithelial cells under microaerobic conditions.FEMS immunology and medical microbiology · 2011Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Gastrointestinal (GI) anthrax, caused by the bacterial infection of Bacillus anthracis, posts a significant bioterrorism threat by its relatively high mortality rate in humans. Different from inhalational anthrax by the route of infection, accumulating evidence indicates the bypass of vegetative bacteria across GI epithelium is required to initiate GI anthrax. Previously, we reported that purified anthrolysin O (ALO), instead of tripartite anthrax edema and lethal toxins, is capable of disrupting gut epithelial tight junctions and barrier function in cultured cells. Here, we show that ALO can disrupt intestinal tissue barrier function in an ex vivo mouse model. To explore the effects of ALO in a cell culture model of B. anthracis infection, we showed that anthrax bacteria can effectively reduce the monolayer integrity of human Caco-2 brush-border expressor (C2BBE) cells based on the reduced transepithelial resistance and the increased leakage of fluorescent dye. This disruption is likely caused by tight junction dysfunction observed by the reorganization of the tight junction protein occludin. Consequently, we observe significant passage of vegetative anthrax bacteria across C2BBE cells. This barrier disruption and bacterial crossover requires ALO since ALO-deficient B. anthracis strains fail to induce monolayer dysfunction and allow the passage of anthrax bacteria. Together these findings point to a pivotal role for ALO within the establishment of GI anthrax infection and the initial bypass of the epithelial barrier.
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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.