ArticleInfection and immunity2011
Clostridium perfringens iota-toxin b induces rapid cell necrosis.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 50 citations in OpenAlex.
- Step-by-step maturation mechanism of the binary toxin pore revealed by cryo-EM analysis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Structural basis for independent pore function of Vpb4 from Bacillus thuringiensis.Nature communications · 2026Article
- Serine clamp of Clostridium perfringens binary toxin BECb (CPILEb)-pore confers cytotoxicity and enterotoxicity.Communications biology · 2025Article
- Cellular Uptake and Cytotoxicity ofToxins · 2023Review
- Phenotypic and Genotypic Characterization ofVeterinary sciences · 2022Article
- The Pore-Forming Subunit C2IIa of the BinaryFrontiers in pharmacology · 2022Article
- Article
- Effects of HMGB1 on Tricellular Tight Junctions via TGF-β Signaling in Human Nasal Epithelial Cells.International journal of molecular sciences · 2021Article
- Article
- Intoxication of mammalian cells with binary clostridial enterotoxins is inhibited by the combination of pharmacological chaperone inhibitors.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Epithelial barrier dysfunction and cell migration induction via JNK/cofilin/actin by angubindin-1.Tissue barriers · 2020Article
- Tricellular tight junction protein LSR/angulin-1 contributes to the epithelial barrier and malignancy in human pancreatic cancer cell line.Histochemistry and cell biology · 2020Article
- Potential for Tight Junction Protein-Directed Drug Development Using Claudin Binders and Angubindin-1.International journal of molecular sciences · 2019Review
- Interaction ofToxins · 2018Article
- Mechanisms of Action and Cell Death Associated withToxins · 2018Review
- Article
- Evaluation of the Epithelial Barrier Function and Ileal Microbiome in an Established Necrotic Enteritis Challenge Model in Broiler Chickens.Frontiers in veterinary science · 2018Article
- Cellular Entry of Clostridium perfringens Iota-Toxin and Clostridium botulinum C2 Toxin.Toxins · 2017Review
- Cellular Uptake of Clostridium botulinum C2 Toxin Requires Acid Sphingomyelinase Activity.Infection and immunity · 2017Article
- Crystal structure and structure-based mutagenesis of actin-specific ADP-ribosylating toxin CPILE-a as novel enterotoxin.PloS one · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clostridium perfringens iota-toxin is a binary toxin composed of an enzyme component (Ia) and a binding component (Ib). Each component alone lacks toxic activity, but together they produce cytotoxic effects. We examined the cytotoxicity of iota-toxin Ib in eight cell lines. A431 and A549 cells were susceptible to Ib, but MDCK, Vero, CHO, Caco-2, HT-29, and DLD-1 cells were not. Ib bound and formed oligomers in the membranes of A431 and MDCK cells. However, Ib entered MDCK cells but not A431 cells, suggesting that uptake is essential for cellular survival. Ib also induced cell swelling and the rapid depletion of cellular ATP in A431 and A549 cells but not the insensitive cell lines. In A431 cells, Ib binds and oligomerizes mainly in nonlipid rafts in the membranes. Disruption of lipid rafts by methyl-β-cyclodextrin did not impair ATP depletion or cell death caused by Ib. Ib induced permeabilization by propidium iodide without DNA fragmentation in A431 cells. Ultrastructural studies revealed that A431 cells undergo necrosis after treatment with Ib. Ib caused a disruption of mitochondrial permeability and the release of cytochrome c. Staining with active-form-specific antibodies showed that the proapoptotic Bcl-2-family proteins Bax and Bak were activated and colocalized with mitochondria in Ib-treated A431 cells. We demonstrate that Ib by itself produces cytotoxic activity through necrosis.
Indexed as
Identifiers
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.