ArticleInfection and immunity2012
Bacillus anthracis lethal toxin reduces human alveolar epithelial barrier function.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 28 citations in OpenAlex.
- From pathogenicity to therapy: Investigating the Therapeutic Potential of Bacillus anthracis Anthrax Toxin in Novel Cancer Therapies and Oncological Research.Archives of microbiology · 2025Review
- In Vivo Comparison of Branched vs Linear Pegylation of a Capsule-Degrading Enzyme for Treatment of Anthrax.ACS omega · 2025Article
- Article
- Bacillus anthracis spores are internalized in human lung epithelial cells by Rab GTPase-supported macropinocytosis.Microbial pathogenesis · 2023Article
- The subversion of toll-like receptor signaling by bacterial and viral proteases during the development of infectious diseases.Molecular aspects of medicine · 2022Review
- Tight Junctions, the Epithelial Barrier, and Toll-like Receptor-4 During Lung Injury.Inflammation · 2022Review
- RUNX3-dependent oxidative epithelial-to-mesenchymal transition in methamphetamine-induced chronic lung injury.Cell stress & chaperones · 2020Article
- 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
- A High-Throughput System for Cyclic Stretching of Precision-Cut Lung Slices During Acute Cigarette Smoke Extract Exposure.Frontiers in physiology · 2020Article
- Article
- Gene expression profiling of primary human type I alveolar epithelial cells exposed to Bacillus anthracis spores reveals induction of neutrophil and monocyte chemokines.Microbial pathogenesis · 2018Article
- Bacillus anthracis spore movement does not require a carrier cell and is not affected by lethal toxin in human lung models.Microbes and infection · 2016Article
- RIG-I and TLR3 are both required for maximum interferon induction by influenza virus in human lung alveolar epithelial cells.Virology · 2015Article
- Desmosomes in acquired disease.Cell and tissue research · 2015Review
- Crossing of the epithelial barriers by Bacillus anthracis: the Known and the Unknown.Frontiers in microbiology · 2015Review
- Bacillus cereus Certhrax ADP-ribosylates vinculin to disrupt focal adhesion complexes and cell adhesion.The Journal of biological chemistry · 2014Article
- Bacillus anthracis has two independent bottlenecks that are dependent on the portal of entry in an intranasal model of inhalational infection.Infection and immunity · 2013Article
- The sepsis model: an emerging hypothesis for the lethality of inhalation anthrax.Journal of cellular and molecular medicine · 2013Article
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 3 countries.
Funding
Abstract
The lung is the site of entry for Bacillus anthracis in inhalation anthrax, the deadliest form of the disease. Bacillus anthracis produces virulence toxins required for disease. Alveolar macrophages were considered the primary target of the Bacillus anthracis virulence factor lethal toxin because lethal toxin inhibits mouse macrophages through cleavage of MEK signaling pathway components, but we have reported that human alveolar macrophages are not a target of lethal toxin. Our current results suggest that, unlike human alveolar macrophages, the cells lining the respiratory units of the lung, alveolar epithelial cells, are a target of lethal toxin in humans. Alveolar epithelial cells expressed lethal toxin receptor protein, bound the protective antigen component of lethal toxin, and were subject to lethal-toxin-induced cleavage of multiple MEKs. These findings suggest that human alveolar epithelial cells are a target of Bacillus anthracis lethal toxin. Further, no reduction in alveolar epithelial cell viability was observed, but lethal toxin caused actin rearrangement and impaired desmosome formation, consistent with impaired barrier function as well as reduced surfactant production. Therefore, by compromising epithelial barrier function, lethal toxin may play a role in the pathogenesis of inhalation anthrax by facilitating the dissemination of Bacillus anthracis from the lung in early disease and promoting edema in late stages of the illness.
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What OpenQuestion holds
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.