ArticleJCI insight2018
Necroptosis of infiltrated macrophages drives Yersinia pestis dispersal within buboes.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- HIGH DOSE GAMMAHERPESVIRUS INFECTION IN MACROPHAGES RESULTS IN INFLAMMATORY MULTIMODAL CELL DEATH.bioRxiv : the preprint server for biology · 2026Article
- Human genetic variation reveals FCRL3 is a lymphocyte receptor for Yersinia pestis.Cell genomics · 2025Article
- Regulation of RIPK1 Phosphorylation: Implications for Inflammation, Cell Death, and Therapeutic Interventions.Biomedicines · 2024Review
- Macrophage innate immune responses delineate between defective translocon assemblies produced byVirulence · 2023Article
- Article
- Pathogenic Exploitation of Lymphatic Vessels.Cells · 2022Review
- Heightened Virulence ofInfection and immunity · 2021Article
- Role of Apoptotic Cell Clearance in Pneumonia and Inflammatory Lung Disease.Pathogens (Basel, Switzerland) · 2021Review
- Plague Transmission from Corpses and Carcasses.Emerging infectious diseases · 2021Review
- miR-425-5p improves inflammation and septic liver damage through negatively regulating the RIP1-mediated necroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
- Difference in Strain Pathogenicity of Septicemic Yersinia pestis Infection in a TLR2Infection and immunity · 2020Article
- Programmed Cell Death in the Evolutionary Race against Bacterial Virulence Factors.Cold Spring Harbor perspectives in biology · 2020Review
- Emerging Evasion Mechanisms of Macrophage Defenses by Pathogenic Bacteria.Frontiers in cellular and infection microbiology · 2020Review
- The involvement of regulated cell death forms in modulating the bacterial and viral pathogenesis.International review of cell and molecular biology · 2020Review
- Programmed necrotic cell death of macrophages: Focus on pyroptosis, necroptosis, and parthanatos.Redox biology · 2019Review
- Yersinia pestis and plague: an updated view on evolution, virulence determinants, immune subversion, vaccination, and diagnostics.Genes and immunity · 2019Review
- Sphingosine-1-Phosphate and Macrophage Biology-How the Sphinx Tames the Big Eater.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
When draining lymph nodes become infected by Yersinia pestis (Y. pestis), a massive influx of phagocytic cells occurs, resulting in distended and necrotic structures known as buboes. The bubonic stage of the Y. pestis life cycle precedes septicemia, which is facilitated by trafficking of infected mononuclear phagocytes through these buboes. However, how Y. pestis convert these immunocytes recruited by host to contain the pathogen into vehicles for bacterial dispersal and the role of immune cell death in this context are unknown. We show that the lymphatic spread requires Yersinia outer protein J (YopJ), which triggers death of infected macrophages by downregulating a suppressor of receptor-interacting protein kinase 1-mediated (RIPK1-mediated) cell death programs. The YopJ-triggered cell death was identified as necroptotic, which released intracellular bacteria, allowing them to infect new neighboring cell targets. Dying macrophages also produced chemotactic sphingosine 1-phosphate, enhancing cell-to-cell contact, further promoting infection. This necroptosis-driven expansion of infected macrophages in buboes maximized the number of bacteria-bearing macrophages reaching secondary lymph nodes, leading to sepsis. In support, necrostatins confined bacteria within macrophages and protected mice from lethal infection. These findings define necrotization of buboes as a mechanism for bacterial spread and a potential target for therapeutic intervention.
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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.