ArticleThe American journal of pathology2007
Clostridium sordellii lethal toxin kills mice by inducing a major increase in lung vascular permeability.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- De novo design of potent inhibitors of clostridial family toxins.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- FatalPathogens (Basel, Switzerland) · 2025Review
- Overview of Bacterial Protein Toxins from Pathogenic Bacteria: Mode of Action and Insights into Evolution.Toxins · 2024Review
- Structural dynamics of the CROPs domain control stability and toxicity of Paeniclostridium sordellii lethal toxin.Nature communications · 2023Article
- Identification of TFPI as a receptor reveals recombination-driven receptor switching in Clostridioides difficile toxin B variants.Nature communications · 2022Article
- Paeniclostridium sordellii uterine infection is dependent on the estrous cycle.PLoS pathogens · 2022Article
- Categorizing Sequences of Concern by Function To Better Assess Mechanisms of Microbial Pathogenesis.Infection and immunity · 2022Review
- Large Clostridial Toxins: Mechanisms and Roles in Disease.Microbiology and molecular biology reviews : MMBR · 2021Review
- Inhibition of Rac1 GTPase Decreases Vascular Oxidative Stress, Improves Endothelial Function, and Attenuates Atherosclerosis Development in Mice.Frontiers in cardiovascular medicine · 2021Article
- Article
- Genome-Wide CRISPR Screen Identifies Semaphorin 6A and 6B as Receptors for Paeniclostridium sordellii Toxin TcsL.Cell host & microbe · 2020Article
- Article
- Experimental identification and computational characterization of a novel extracellular metalloproteinase produced byRSC advances · 2017Article
- Article
- Fatal Spontaneous Clostridium bifermentans Necrotizing Endometritis: A Case Report and Literature Review of the Pathogen.Open forum infectious diseases · 2016Article
- A novel murine model of Clostridium sordellii myonecrosis: Insights into the pathogenesis of disease.Anaerobe · 2016Article
- Foot infection by Clostridium sordellii: case report and review of 15 cases in France.Journal of clinical microbiology · 2015Article
- Diet-induced alterations in gut microflora contribute to lethal pulmonary damage in TLR2/TLR4-deficient mice.Cell reports · 2014Article
- Bacterial factors exploit eukaryotic Rho GTPase signaling cascades to promote invasion and proliferation within their host.Small GTPases · 2014Review
- Development of ELISA based detection system for lethal toxin of Clostridium sordellii.The Indian journal of medical research · 2013Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
When intraperitoneally injected into Swiss mice, Clostridium sordellii lethal toxin reproduces the fatal toxic shock syndrome observed in humans and animals after natural infection. This animal model was used to study the mechanism of lethal toxin-induced death. Histopathological and biochemical analyses identified lung and heart as preferential organs targeted by lethal toxin. Massive extravasation of blood fluid in the thoracic cage, resulting from an increase in lung vascular permeability, generated profound modifications such as animal dehydration, increase in hematocrit, hypoxia, and finally, cardiorespiratory failure. Vascular permeability increase induced by lethal toxin resulted from modifications of lung endothelial cells as evidenced by electron microscopy. Immunohistochemical analysis demonstrated that VE-cadherin, a protein participating in intercellular adherens junctions, was redistributed from membrane to cytosol in lung endothelial cells. No major sign of lethal toxin-induced inflammation was observed that could participate in the toxic shock syndrome. The main effect of the lethal toxin is the glucosylation-dependent inactivation of small GTPases, in particular Rac, which is involved in actin polymerization occurring in vivo in lungs leading to E-cadherin junction destabilization. We conclude that the cells most susceptible to lethal toxin are lung vascular endothelial cells, the adherens junctions of which were altered after intoxication.
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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.