ArticleInfection and immunity2011
Mutagenic analysis of the Clostridium difficile flagellar proteins, FliC and FliD, and their contribution to virulence in hamsters.
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 82 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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Who cites it
82 citing papers in PubMed, 144 citations in OpenAlex.
- From colonization to infection: Genomic evolution of Clostridioides difficile pathogenesis.Cell reports · 2026Review
- A longitudinal analysis of Clostridioides difficile virulence profiles across three geographic regions in Israel (2020-2022).Annals of clinical microbiology and antimicrobials · 2026Article
- Do Human-InfectingPathogens (Basel, Switzerland) · 2026Article
- How flagellar glycosylation of the phytopathogenic bacteriumApplied and environmental microbiology · 2026Article
- Dissecting the role of flagellar subunits inJournal of bacteriology · 2025Article
- Flagellar switch inverted repeats impact heterogeneity in flagellar gene expression and thus C. difficile RT027/MLST1 virulence.Cell reports · 2025Article
- Naringenin targets FimZ to regulate type I fimbriae and reduce the virulence ofFrontiers in cellular and infection microbiology · 2025Article
- In-depth characterization of accessory gene regulator loci and associated virulence factors inCurrent research in microbial sciences · 2025Article
- VmsR, a LuxR-Type Regulator, Contributes to Virulence, Cell Motility, Extracellular Polysaccharide Production and Biofilm Formation inInternational journal of molecular sciences · 2024Article
- Environmental and Nutritional Parameters Modulating Genetic Expression for Virulence Factors ofAntibiotics (Basel, Switzerland) · 2024Review
- Review
- Characterization of the Clostridioides difficile 630Δerm putative Pro-Pro endopeptidase CD1597.Access microbiology · 2024Article
- Immunization Strategies Against Clostridioides difficile.Advances in experimental medicine and biology · 2024Review
- Revised Model for the Type A Glycan Biosynthetic Pathway inACS infectious diseases · 2023Article
- Biofilm Formation ofMicroorganisms · 2023Review
- Recombinant Fusion Protein Vaccine Containing Clostridioides difficile FliC and FliD Protects Mice against C. difficile Infection.Infection and immunity · 2023Article
- Review
- Impact of Subinhibitory Concentrations of Metronidazole on Morphology, Motility, Biofilm Formation and Colonization ofAntibiotics (Basel, Switzerland) · 2022Article
- Regulation of Clostridioides difficile toxin production.Current opinion in microbiology · 2022Review
- Destination and Specific Impact of Different Bile Acids in the Intestinal PathogenFrontiers in microbiology · 2022Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although toxins A and B are known to be important contributors to the acute phase of Clostridium difficile infection, the role of colonization and adherence to host tissues in the overall pathogenesis of these organisms remains unclear. Consequently, we used the recently introduced intron-based ClosTron gene interruption system to eliminate the expression of two reported C. difficile colonization factors, the major flagellar structural subunit (FliC) and the flagellar cap protein (FliD), to gain greater insight into how flagella and motility contribute to C. difficile's pathogenic strategy. The results demonstrate that interrupting either the fliC or the fliD gene results in a complete loss of flagella, as well as motility, in C. difficile. However, both the fliC and fliD mutant strains adhered better than the wild-type 630Δerm strain to human intestine-derived Caco-2 cells, suggesting that flagella and motility do not contribute to, or may even interfere with, C. difficile adherence to epithelial cell surfaces in vitro. Moreover, we found that the mutant strains were more virulent in hamsters, indicating either that flagella are unnecessary for virulence or that repression of motility may be a pathogenic strategy employed by C. difficile in hamsters.
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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.