ArticlePLoS pathogens2013
The cytotoxic necrotizing factor of Yersinia pseudotuberculosis (CNFY) enhances inflammation and Yop delivery during infection by activation of Rho GTPases.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 73 citations in OpenAlex.
- Unraveling the Pathogenetic Potential and Immune Crosstalk of Yersinia spp. in Inflammatory Bowel Disease.Journal of immunology research · 2026Review
- Interkingdom sensing of fungal tyrosol promotes bacterial antifungal T6SS activity in the murine gut.Nature microbiology · 2026Article
- A Fur-regulated type VI secretion system contributes to oxidative stress resistance and virulence in Yersinia pseudotuberculosis.Stress biology · 2023Article
- Cpx-signalling facilitates Hms-dependent biofilm formation by Yersinia pseudotuberculosis.NPJ biofilms and microbiomes · 2022Article
- Which bacterial toxins are worthy of validation as markers in colorectal cancer screening? A critical review.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2022Review
- Induction of Filopodia During Cytomegalovirus Entry Into Human Iris Stromal Cells.Frontiers in microbiology · 2022Article
- Role of the Yersinia pseudotuberculosis Virulence Plasmid in Pathogen-Phagocyte Interactions in Mesenteric Lymph Nodes.EcoSal Plus · 2021Review
- The Cytotoxic Necrotizing Factors (CNFs)-A Family of Rho GTPase-Activating Bacterial Exotoxins.Toxins · 2021Review
- γδ T cell IFNγ production is directly subverted by Yersinia pseudotuberculosis outer protein YopJ in mice and humans.PLoS pathogens · 2021Article
- The gatekeeper of Yersinia type III secretion is under RNA thermometer control.PLoS pathogens · 2021Article
- T6SS translocates a micropeptide to suppress STING-mediated innate immunity by sequestering manganese.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- A simple nuclear contrast staining method for microCT-based 3D histology using lead(II) acetate.Journal of anatomy · 2021Article
- Crystal structure of bacterial cytotoxic necrotizing factor CNFThe EMBO journal · 2021Article
- Aerobactin-Mediated Iron Acquisition Enhances Biofilm Formation, Oxidative Stress Resistance, and Virulence ofFrontiers in microbiology · 2021Article
- Far Eastern Scarlet-Like Fever is a Special Clinical and Epidemic Manifestation ofPathogens (Basel, Switzerland) · 2020Review
- An RNA thermometer dictates production of a secreted bacterial toxin.PLoS pathogens · 2020Article
- A bacterial secreted translocator hijacks riboregulators to control type III secretion in response to host cell contact.PLoS pathogens · 2019Article
- Unraveling neutrophil-F1000Research · 2019Review
- Article
- Visualization of translocons in Yersinia type III protein secretion machines during host cell infection.PLoS pathogens · 2018Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Some isolates of Yersinia pseudotuberculosis produce the cytotoxic necrotizing factor (CNFY), but the functional consequences of this toxin for host-pathogen interactions during the infection are unknown. In the present study we show that CNFY has a strong influence on virulence. We demonstrate that the CNFY toxin is thermo-regulated and highly expressed in all colonized lymphatic tissues and organs of orally infected mice. Most strikingly, we found that a cnfY knock-out variant of a naturally toxin-expressing Y. pseudotuberculosis isolate is strongly impaired in its ability to disseminate into the mesenteric lymph nodes, liver and spleen, and has fully lost its lethality. The CNFY toxin contributes significantly to the induction of acute inflammatory responses and to the formation of necrotic areas in infected tissues. The analysis of the host immune response demonstrated that presence of CNFY leads to a strong reduction of professional phagocytes and natural killer cells in particular in the spleen, whereas loss of the toxin allows efficient tissue infiltration of these immune cells and rapid killing of the pathogen. Addition of purified CNFY triggers formation of actin-rich membrane ruffles and filopodia, which correlates with the activation of the Rho GTPases, RhoA, Rac1 and Cdc42. The analysis of type III effector delivery into epithelial and immune cells in vitro and during the course of the infection further demonstrated that CNFY enhances the Yop translocation process and supports a role for the toxin in the suppression of the antibacterial host response. In summary, we highlight the importance of CNFY for pathogenicity by showing that this toxin modulates inflammatory responses, protects the bacteria from attacks of innate immune effectors and enhances the severity of a Yersinia infection.
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