ArticlePloS one2014
Clostridium perfringens phospholipase C induced ROS production and cytotoxicity require PKC, MEK1 and NFκB activation.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- Prebiotic supplementation modulates advanced glycation end-products (AGEs), soluble receptor for AGEs (sRAGE), and cardiometabolic risk factors through improving metabolic endotoxemia: a randomized-controlled clinical trial.European journal of nutrition · 2020Trial
- Hoof, Vaginal and Milk Microbiota Alterations in Dairy Cows with Foot Rot.Animals : an open access journal from MDPI · 2026Article
- Article
- The ability of clostridium novyi-NT spores to induce apoptosis via the mitochondrial pathway in mice with HPV-positive cervical cancer tumors derived from the TC-1 cell line.BMC complementary medicine and therapies · 2024Article
- Purinergic Receptor Antagonists Inhibit Hemolysis Induced byPathogens (Basel, Switzerland) · 2024Article
- Article
- Phospholipase C: underrated players in microbial infections.Frontiers in cellular and infection microbiology · 2023Review
- Comparative Genomics ofMicroorganisms · 2022Article
- Bacterial phospholipases C with dual activity: phosphatidylcholinesterase and sphingomyelinase.FEBS open bio · 2021Review
- Article
- Study of the Structure and Biological Activity of the Amino-Terminus of the α-Toxin from Clostridium welchii Type A.Current microbiology · 2019Article
- Histotoxic Clostridial Infections.Microbiology spectrum · 2019Article
- Integrative Analyses of Long Non-coding RNA and mRNA Involved in Piglet Ileum Immune Response toFrontiers in cellular and infection microbiology · 2019Article
- Mechanisms of Action and Cell Death Associated withToxins · 2018Review
- Article
- Melatonin inhibits apoptotic cell death induced by Vibrio vulnificus VvhA via melatonin receptor 2 coupling with NCF-1.Cell death & disease · 2018Article
- Clostridium perfringens α-toxin impairs erythropoiesis by inhibition of erythroid differentiation.Scientific reports · 2017Article
- AFrontiers in cellular and infection microbiology · 2017Article
- Bacterial Sphingomyelinases and Phospholipases as Virulence Factors.Microbiology and molecular biology reviews : MMBR · 2016Review
- Vibrio vulnificus VvhA induces NF-κB-dependent mitochondrial cell death via lipid raft-mediated ROS production in intestinal epithelial cells.Cell death & disease · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clostridium perfringens phospholipase C (CpPLC), also called α-toxin, is the most toxic extracellular enzyme produced by this bacteria and is essential for virulence in gas gangrene. At lytic concentrations, CpPLC causes membrane disruption, whereas at sublytic concentrations this toxin causes oxidative stress and activates the MEK/ERK pathway, which contributes to its cytotoxic and myotoxic effects. In the present work, the role of PKC, ERK 1/2 and NFκB signalling pathways in ROS generation induced by CpPLC and their contribution to CpPLC-induced cytotoxicity was evaluated. The results demonstrate that CpPLC induces ROS production through PKC, MEK/ERK and NFκB pathways, the latter being activated by the MEK/ERK signalling cascade. Inhibition of either of these signalling pathways prevents CpPLC's cytotoxic effect. In addition, it was demonstrated that NFκB inhibition leads to a significant reduction in the myotoxicity induced by intramuscular injection of CpPLC in mice. Understanding the role of these signalling pathways could lead towards developing rational therapeutic strategies aimed to reduce cell death during a clostridialmyonecrosis.
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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.