ArticleScientific reports2019
Dual role of the colonization factor CD2831 in Clostridium difficile pathogenesis.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
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- Whole-genome sequencing of toxigenic Clostridioides difficile reveals multidrug resistance and virulence genes in strains of environmental and animal origin.BMC veterinary research · 2024Article
- Genomic study of EuropeanMicrobial genomics · 2024Article
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- Clostridioides difficile Biofilm.Advances in experimental medicine and biology · 2024Article
- Immunization Strategies Against Clostridioides difficile.Advances in experimental medicine and biology · 2024Review
- Pathogenicity and virulence ofVirulence · 2023Review
- An intact S-layer is advantageous to Clostridioides difficile within the host.PLoS pathogens · 2023Article
- Non-Toxin-BasedPathogens (Basel, Switzerland) · 2023Article
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- Coordinated modulation of multiple processes through phase variation of a c-di-GMP phosphodiesterase in Clostridioides difficile.PLoS pathogens · 2022Article
- Phylogenetic analysis of the bacterial Pro-Pro-endopeptidase domain reveals a diverse family including secreted and membrane anchored proteins.Current research in microbial sciences · 2021Review
- Phase-variable expression of pdcB, a phosphodiesterase, influences sporulation in Clostridioides difficile.Molecular microbiology · 2021Article
- Wolf in Sheep's Clothing:Microorganisms · 2021Review
- Biofilm regulation in Clostridioides difficile: Novel systems linked to hypervirulence.PLoS pathogens · 2021Review
- Prophylaxis and Treatment againstInternational journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clostridium difficile is a Gram-positive, anaerobic bacterium and the leading cause of antibiotic-associated diarrhea and pseudomembranous colitis. C. difficile modulates its transition from a motile to a sessile lifestyle through a mechanism of riboswitches regulated by cyclic diguanosine monophosphate (c-di-GMP). Previously described as a sortase substrate positively regulated by c-di-GMP, CD2831 was predicted to be a collagen-binding protein and thus potentially involved in sessility. By overexpressing CD2831 in C. difficile and heterologously expressing it on the surface of Lactococcus lactis, here we further demonstrated that CD2831 is a collagen-binding protein, able to bind to immobilized collagen types I, III and V as well as native collagen produced by human fibroblasts. We also observed that the overexpression of CD2831 raises the ability to form biofilm on abiotic surface in both C. difficile and L. lactis. Notably, we showed that CD2831 binds to the collagen-like domain of the human complement component C1q, suggesting a role in preventing complement cascade activation via the classical pathway. This functional characterization places CD2831 in the Microbial Surface Components Recognizing Adhesive Matrix Molecule (MSCRAMMs) family, a class of virulence factors with a dual role in adhesion to collagen-rich tissues and in host immune evasion by binding to human complement components.
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