ArticleInfection and immunity2008
Yersinia pestis type III secretion system-dependent inhibition of human polymorphonuclear leukocyte function.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 66 citations in OpenAlex.
- Strategies in immune subversion: How Yersinia pestis inhibits neutrophil responses.PLoS pathogens · 2026Article
- Human genetic variation reveals FCRL3 is a lymphocyte receptor for Yersinia pestis.Cell genomics · 2025Article
- Distinct mechanisms of type 3 secretion system recognition control LTB4 synthesis in neutrophils and macrophages.PLoS pathogens · 2024Article
- Distinct Mechanisms of Type 3 Secretion System Recognition Control LTBbioRxiv : the preprint server for biology · 2024Article
- Type 3 secretion system induced leukotriene B4 synthesis by leukocytes is actively inhibited by Yersinia pestis to evade early immune recognition.PLoS pathogens · 2024Article
- Characterization and CRISPR/Cas9-mediated genetic manipulation of neutrophils derived from Hoxb8-ER-immortalized myeloid progenitors.Journal of leukocyte biology · 2023Article
- Antibody Opsonization Enhances Early Interactions between Yersinia pestis and Neutrophils in the Skin and Draining Lymph Node in a Mouse Model of Bubonic Plague.Infection and immunity · 2020Article
- Yersinia pestis escapes entrapment in thrombi by targeting platelet function.Journal of thrombosis and haemostasis : JTH · 2020Article
- A Dual Role for the Plasminogen Activator Protease During the Preinflammatory Phase of Primary Pneumonic Plague.The Journal of infectious diseases · 2020Article
- Redundant and Cooperative Roles for Yersinia pestis Yop Effectors in the Inhibition of Human Neutrophil Exocytic Responses Revealed by Gain-of-Function Approach.Infection and immunity · 2020Article
- The roles of NADPH oxidase in modulating neutrophil effector responses.Molecular oral microbiology · 2019Review
- Gain-of-Function Analysis Reveals Important Virulence Roles for the Yersinia pestis Type III Secretion System Effectors YopJ, YopT, and YpkA.Infection and immunity · 2018Article
- Induction of Type I Interferon through a Noncanonical Toll-Like Receptor 7 Pathway during Yersinia pestis Infection.Infection and immunity · 2017Article
- Neutrophils to the ROScue: Mechanisms of NADPH Oxidase Activation and Bacterial Resistance.Frontiers in cellular and infection microbiology · 2017Review
- Characterization ofFrontiers in cellular and infection microbiology · 2017Article
- Intramacrophage Infection Reinforces the Virulence of Edwardsiella tarda.Journal of bacteriology · 2016Article
- Role of the Yersinia YopJ protein in suppressing interleukin-8 secretion by human polymorphonuclear leukocytes.Microbes and infection · 2016Article
- Spatially distinct neutrophil responses within the inflammatory lesions of pneumonic plague.mBio · 2015Article
- Adhesive properties of YapV and paralogous autotransporter proteins of Yersinia pestis.Infection and immunity · 2015Article
- Dermal neutrophil, macrophage and dendritic cell responses to Yersinia pestis transmitted by fleas.PLoS pathogens · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Human polymorphonuclear leukocytes (PMNs, or neutrophils) are the primary innate host defense against invading bacterial pathogens. Neutrophils are rapidly recruited to sites of infection and ingest microorganisms through a process known as phagocytosis. Following phagocytosis by human PMNs, microorganisms are killed by reactive oxygen species (ROS) and microbicidal products contained within granules. Yersinia pestis, the causative agent of plague, is capable of rapid replication and dissemination from sites of infection in the host. Although Y. pestis survives in macrophages, the bacterial fate following interaction with human PMNs is less clear. The ability of Y. pestis to inhibit phagocytosis by human PMNs was assessed by differential fluorescence microscopy and was shown to be dependent on expression of the type III secretion system (TTSS). Previous studies have demonstrated that TTSS expression in enteropathogenic Yersinia spp. also inhibits the respiratory burst in PMNs and macrophages, and we show here that human PMN ROS production is similarly repressed by Y. pestis. However, exclusion of uningested TTSS-expressing Y. pestis with gentamicin revealed that intracellular bacteria are eliminated by human PMNs, similar to bacteria lacking the TTSS. In summary, our results suggest that the Y. pestis TTSS contributes to extracellular survival following interactions with human PMNs and that the intracellular fate is independent of TTSS inhibition of neutrophil ROS production.
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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.