ReviewVeterinary microbiology2011
Recent progress in understanding the pathogenesis of Clostridium perfringens type C infections.
Review in Veterinary microbiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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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
33 citing papers in PubMed, 71 citations in OpenAlex.
- Isolation, toxin gene profiling, and phylogenetic analysis of Clostridium perfringens in Egyptian fruit bats: public health and epidemiological implications.Scientific reports · 2025Article
- Molecular characterization and function of JAK/STAT pathway in IPEC-J2 cells during Clostridium perfringens beta2 toxin stimulation.Veterinary research communications · 2023Article
- Change in Long Non-Coding RNA Expression Profile Related to the Antagonistic Effect ofCurrent issues in molecular biology · 2023Article
- Effects of three different probiotics of Tibetan sheep origin and their complex probiotics on intestinal damage, immunity, and immune signaling pathways of mice infected withFrontiers in microbiology · 2023Article
- Biofilm formation, antimicrobial assay, and toxin-genotypes of Clostridium perfringens type C isolates cultured from a neonatal Yangtze finless porpoise.Archives of microbiology · 2022Article
- Phenotypic and Genotypic Characterization ofVeterinary sciences · 2022Article
- TMT labeled comparative proteomic analysis reveals spleen active immune responses duringPeerJ · 2022Article
- Article
- Pathogenicity and virulence ofVirulence · 2021Article
- Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc · 2020Review
- Identification and Characterization of MAPK Signaling Pathway Genes and Associated lncRNAs in the Ileum of Piglets Infected byBioMed research international · 2020Article
- Shifts in the Fecal Microbial Community ofFrontiers in microbiology · 2020Article
- Histological and Comparative Transcriptome Analyses Provide Insights into Small Intestine Health in Diarrheal Piglets after Infection withAnimals : an open access journal from MDPI · 2019Article
- Article
- Vaccination againstPorcine health management · 2019Article
- Review
- Circular RNA expression profile of spleen in aFEBS open bio · 2018Article
- Vaccines as alternatives to antibiotics for food producing animals. Part 2: new approaches and potential solutions.Veterinary research · 2018Review
- Analyses of long non-coding RNA and mRNA profiling in the spleen of diarrheic piglets caused byPeerJ · 2018Article
- Native or Proteolytically Activated NanI Sialidase Enhances the Binding and Cytotoxic Activity of Clostridium perfringens Enterotoxin and Beta Toxin.Infection and immunity · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Clostridium perfringens type C causes necrotizing enteritis in humans and several other animal species. Type C isolates must produce at least beta toxin (CPB) and alpha toxin (CPA) and most strains produce several other toxins including perfringolysin O (PFO) and TpeL. However, current evidence indicates that CPB is the main virulence factor for type C infections. Most of this evidence is based upon the loss of virulence shown by isogenic type C CPB knock out mutants on cells, and also in rabbit intestinal loops and in mouse models. This virulence is regained when these mutants are complemented with the wild-type cpb gene. 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.
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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.