ArticleCellular microbiology2009
Contact with enterocyte-like Caco-2 cells induces rapid upregulation of toxin production by Clostridium perfringens type C isolates.
Article in Cellular microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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.
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.
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Who cites it
42 citing papers in PubMed, 65 citations in OpenAlex.
- Integrated transcriptomics and metabolomics reveal multi-target mechanisms of tannins against Clostridium perfringens and necrotic enteritis.Journal of animal science and biotechnology · 2025Article
- The presence of differentiated C2C12 muscle cells enhances toxin production and growth byVirulence · 2024Article
- The Effect of Caco-2 Cells on Sporulation and Enterotoxin Expression by FoodbornePathogens (Basel, Switzerland) · 2024Article
- Expression of α- and ε-toxin genes inIranian journal of veterinary research · 2022Article
- A Poultry Subclinical Necrotic Enteritis Disease Model Based on NaturalFrontiers in physiology · 2022Article
- Identifying the Basis for VirS/VirR Two-Component Regulatory System Control of Clostridium perfringens Beta-Toxin Production.Journal of bacteriology · 2021Article
- Alginate Nanoparticles Enhance Anti-Clostridium perfringens Activity of the Leaderless Two-Peptide Enterocin DD14 and Affect Expression of Some Virulence Factors.Probiotics and antimicrobial proteins · 2021Article
- Pathogenic Characterization ofFrontiers in microbiology · 2021Article
- Article
- Article
- The Agr-Like Quorum Sensing System Is Required for Pathogenesis of Necrotic Enteritis Caused by Clostridium perfringens in Poultry.Infection and immunity · 2017Article
- Rethinking the role of alpha toxin in Clostridium perfringens-associated enteric diseases: a review on bovine necro-haemorrhagic enteritis.Veterinary research · 2017Review
- Simulating Intestinal Growth Conditions Enhances Toxin Production of EnteropathogenicFrontiers in microbiology · 2017Article
- Review
- The CpAL quorum sensing system regulates production of hemolysins CPA and PFO to build Clostridium perfringens biofilms.Infection and immunity · 2015Article
- Clostridium perfringens type A-E toxin plasmids.Research in microbiology · 2015Review
- Structure-function analysis of peptide signaling in the Clostridium perfringens Agr-like quorum sensing system.Journal of bacteriology · 2015Article
- Article
- Review
- Virulence Plasmids of Spore-Forming Bacteria.Microbiology spectrum · 2014Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
Abstract
Clostridium perfringens type C isolates cause necrotizing enteritis in humans and domestic animals. In vitro, type C isolates often produce beta toxin (CPB), beta2 toxin (CPB2), alpha toxin (CPA), perfringolysin O (PFO) and TpeL during (or after) late log-phase growth. In contrast, the current study found that many type C isolates respond to close contact with enterocyte-like Caco-2 cells by producing all toxins, except TpeL, much more rapidly than occurs during in vitro growth. This in vivo effect involves rapid transcriptional upregulation of the cpb, cpb2, pfoA and plc toxin genes. Rapid Caco-2 cell-induced upregulation of CPB and PFO production involves the VirS/VirR two-component system, since upregulated in vivo transcription of the pfoA and cpb genes was blocked by inactivating the virR gene and was reversible by complementation to restore VirR expression. However, the luxS quorum-sensing system is not required for the rapid upregulation of type C toxin production induced by contact with Caco-2 cells. These results provide the first indication of host cell:pathogen cross-talk affecting toxin production kinetics by any pathogenic Clostridium spp., identify in vivo versus in vitro differences in C. perfringens toxin expression, and implicate VirS/VirR as a possible contributor to some C. perfringens enteric diseases.
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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.