ArticleToxins2015
The pore-forming α-toxin from clostridium septicum activates the MAPK pathway in a Ras-c-Raf-dependent and independent manner.
Article in Toxins, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Case Report: A case of severe infection caused byFrontiers in medicine · 2026Article
- Advances in gut microbiota-related treatment strategies for managing colorectal cancer in humans.Cancer biology & medicine · 2025Review
- Confinement energy landscape classification reveals membrane receptor nano-organization mechanisms.Biophysical journal · 2024Article
- Anti-tumor Effects of Recombinant Clostridium α-Toxin on Breast Cancer: AnInternational journal of molecular and cellular medicine · 2024Article
- Review
- Membrane repair triggered by cholesterol-dependent cytolysins is activated by mixed lineage kinases and MEK.Science advances · 2022Article
- Relationships between gut microbiota, red meat consumption and colorectal cancer.Journal of carcinogenesis & mutagenesis · 2022Article
- Gut microbiota-derived metabolites in CRC progression and causation.Journal of cancer research and clinical oncology · 2021Review
- Panorama of the Intracellular Molecular Concert Orchestrated by Actinoporins, Pore-Forming Toxins from Sea Anemones.Toxins · 2021Review
- First Comparative Analysis ofFrontiers in microbiology · 2021Article
- Improvement in the Growth and α-toxin Production of Clostridium septicum by Magnesium Sulfate.Archives of Razi Institute · 2020Article
- Review
- Histotoxic Clostridial Infections.Microbiology spectrum · 2019Article
- Transcriptomic analysis ofBiology open · 2019Article
- Article
- Microbiota, Inflammation and Colorectal Cancer.International journal of molecular sciences · 2017Review
- Complete Genome Sequence of Clostridium septicum Strain CSUR P1044, Isolated from the Human Gut Microbiota.Genome announcements · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clostridium septicum is the causative agent of atraumatic gas gangrene, with α-toxin, an extracellular pore-forming toxin, essential for disease. How C. septicum modulates the host's innate immune response is poorly defined, although α-toxin-intoxicated muscle cells undergo cellular oncosis, characterised by mitochondrial dysfunction and release of reactive oxygen species. Nonetheless, the signalling events that occur prior to the initiation of oncosis are poorly characterised. Our aims were to characterise the ability of α-toxin to activate the host mitogen activated protein kinase (MAPK) signalling pathway both in vitro and in vivo. Treatment of Vero cells with purified α-toxin activated the extracellular-signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 arms of the MAPK pathway and stimulated the release of TNF-α in a dose-dependent manner. Studies using inhibitors of all three MAPK components suggested that activation of ERK occurred in a Ras-c-Raf dependent manner, whereas activation of JNK and p38 occurred by a Ras-independent mechanism. Toxin-mediated activation was dependent on efficient receptor binding and pore formation and on an influx of extracellular calcium ions. In the mouse myonecrosis model we showed that the MAPK pathway was activated in tissues of infected mice, implying that it has an important role in the disease process.
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Registered trials
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