ArticlePLoS pathogens2018
Loss of CNFY toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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
14 citing papers in PubMed, 32 citations in OpenAlex.
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- Yersinia pseudotuberculosis doxycycline tolerance strategies include modulating expression of genes involved in cell permeability and tRNA modifications.PLoS pathogens · 2022Article
- Bacterial AB toxins and host-microbe interactions.Advances in microbial physiology · 2022Review
- The Cytotoxic Necrotizing Factors (CNFs)-A Family of Rho GTPase-Activating Bacterial Exotoxins.Toxins · 2021Review
- Role of the Yersinia pseudotuberculosis Virulence Plasmid in Pathogen-Phagocyte Interactions in Mesenteric Lymph Nodes.EcoSal Plus · 2021Review
- Yersinia remodels epigenetic histone modifications in human macrophages.PLoS pathogens · 2021Article
- Crystal structure of bacterial cytotoxic necrotizing factor CNFThe EMBO journal · 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
- Article
- Discovering RNA-Based Regulatory Systems forFrontiers in cellular and infection microbiology · 2018Review
- AllFrontiers in cellular and infection microbiology · 2018Review
Corrections and comments
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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
Gastrointestinal infections caused by enteric yersiniae can become persistent and complicated by relapsing enteritis and severe autoimmune disorders. To establish a persistent infection, the bacteria have to cope with hostile surroundings when they transmigrate through the intestinal epithelium and colonize underlying gut-associated lymphatic tissues. How the bacteria gain a foothold in the face of host immune responses is poorly understood. Here, we show that the CNFY toxin, which enhances translocation of the antiphagocytic Yop effectors, induces inflammatory responses. This results in extensive tissue destruction, alteration of the intestinal microbiota and bacterial clearance. Suppression of CNFY function, however, increases interferon-γ-mediated responses, comprising non-inflammatory antimicrobial activities and tolerogenesis. This process is accompanied by a preterm reprogramming of the pathogen's transcriptional response towards persistence, which gives the bacteria a fitness edge against host responses and facilitates establishment of a commensal-type life style.
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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.