ArticlePLoS pathogens2013
Early apoptosis of macrophages modulated by injection of Yersinia pestis YopK promotes progression of primary pneumonic plague.
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 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
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- Buprenorphine extended-release (Ethiqa XR) impacts the immunological response in mice exposed to aerosolizedFrontiers in immunology · 2026Article
- Pathogenicity and virulence ofVirulence · 2024Review
- Pneumonic Plague Protection Induced by a Monophosphoryl Lipid A Decorated Yersinia Outer-Membrane-Vesicle Vaccine.Small (Weinheim an der Bergstrasse, Germany) · 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
- Protection Induced by Oral Vaccination with a RecombinantInfection and immunity · 2022Article
- Modification of the Pulmonary MyD88 Inflammatory Response Underlies the Role of the Yersinia pestis Pigmentation Locus in Primary Pneumonic Plague.Infection and immunity · 2021Article
- VscF in T3SS1 Helps to Translocate VPA0226 inFrontiers in cellular and infection microbiology · 2021Article
- Bacteroides fragilis Strain ZY-312 Defense against Cronobacter sakazakii-Induced Necrotizing EnterocolitismSystems · 2019Article
- Yersinia pestis and plague: an updated view on evolution, virulence determinants, immune subversion, vaccination, and diagnostics.Genes and immunity · 2019Review
- Metabolomic analyses reveal lipid abnormalities and hepatic dysfunction in non-human primate model for Yersinia pestis.Metabolomics : Official journal of the Metabolomic Society · 2018Article
- 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
- IL-7 suppresses macrophage autophagy and promotes liver pathology in Schistosoma japonicum-infected mice.Journal of cellular and molecular medicine · 2018Article
- Centrality in the host-pathogen interactome is associated with pathogen fitness during infection.Nature communications · 2017Article
- New Role for FDA-Approved Drugs in Combating Antibiotic-Resistant Bacteria.Antimicrobial agents and chemotherapy · 2016Article
- Temporal Progression of Pneumonic Plague in Blood of Nonhuman Primate: A Transcriptomic Analysis.PloS one · 2016Article
- Macrophage cell death upon intracellular bacterial infection.Macrophage · 2015Article
- Further characterization of a highly attenuated Yersinia pestis CO92 mutant deleted for the genes encoding Braun lipoprotein and plasminogen activator protease in murine alveolar and primary human macrophages.Microbial pathogenesis · 2015Article
- Article
- Host response during Yersinia pestis infection of human bronchial epithelial cells involves negative regulation of autophagy and suggests a modulation of survival-related and cellular growth pathways.Frontiers in microbiology · 2015Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Yersinia pestis causes pneumonic plague, a disease characterized by inflammation, necrosis and rapid bacterial growth which together cause acute lung congestion and lethality. The bacterial type III secretion system (T3SS) injects 7 effector proteins into host cells and their combined activities are necessary to establish infection. Y. pestis infection of the lungs proceeds as a biphasic inflammatory response believed to be regulated through the control of apoptosis and pyroptosis by a single, well-conserved T3SS effector protein YopJ. Recently, YopJ-mediated pyroptosis, which proceeds via the NLRP3-inflammasome, was shown to be regulated by a second T3SS effector protein YopK in the related strain Y. pseudotuberculosis. In this work, we show that for Y. pestis, YopK appears to regulate YopJ-mediated apoptosis, rather than pyroptosis, of macrophages. Inhibition of caspase-8 blocked YopK-dependent apoptosis, suggesting the involvement of the extrinsic pathway, and appeared cell-type specific. However, in contrast to yopJ, deletion of yopK caused a large decrease in virulence in a mouse pneumonic plague model. YopK-dependent modulation of macrophage apoptosis was observed at 6 and 24 hours post-infection (HPI). When YopK was absent, decreased populations of macrophages and dendritic cells were seen in the lungs at 24 HPI and correlated with resolution rather than progression of inflammation. Together the data suggest that Y. pestis YopK may coordinate the inflammatory response during pneumonic plague through the regulation of apoptosis of immune cells.
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