ArticleInfection and immunity2009
Gr1+ cells control growth of YopM-negative yersinia pestis during systemic plague.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
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Who cites it
39 citing papers in PubMed, 61 citations in OpenAlex.
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- The Diverse Roles of the Global Transcriptional Regulator PhoP in the Lifecycle ofPathogens (Basel, Switzerland) · 2020Review
- Chromosomally-EncodedFrontiers in cellular and infection microbiology · 2019Article
- Unraveling neutrophil-F1000Research · 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
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- AllFrontiers in cellular and infection microbiology · 2018Review
- CD8(+) T cells specific to a single Yersinia pseudotuberculosis epitope restrict bacterial replication in the liver but fail to provide sterilizing immunity.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2016Article
- Distribution and Evolution of Yersinia Leucine-Rich Repeat Proteins.Infection and immunity · 2016Article
- Immunosuppressive Yersinia Effector YopM Binds DEAD Box Helicase DDX3 to Control Ribosomal S6 Kinase in the Nucleus of Host Cells.PLoS pathogens · 2016Article
- Manipulation of Interleukin-1β and Interleukin-18 Production by Yersinia pestis Effectors YopJ and YopM and Redundant Impact on Virulence.The Journal of biological chemistry · 2016Article
- Adh enhances Actinobacillus pleuropneumoniae pathogenicity by binding to OR5M11 and activating p38 which induces apoptosis of PAMs and IL-8 release.Scientific reports · 2016Article
- Yersinia type III effectors perturb host innate immune responses.World journal of biological chemistry · 2016Review
- Yersinia virulence factors - a sophisticated arsenal for combating host defences.F1000Research · 2016Review
- Spatially distinct neutrophil responses within the inflammatory lesions of pneumonic plague.mBio · 2015Article
- Yersinia pestis Requires Host Rab1b for Survival in Macrophages.PLoS pathogens · 2015Article
- Yersinia pestis targets neutrophils via complement receptor 3.Cellular microbiology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
YopM, a protein toxin of Yersinia pestis, is necessary for virulence in a mouse model of systemic plague. We previously reported YopM-dependent natural killer (NK) cell depletion from blood and spleen samples of infected mice. However, in this study we found that infection with Y. pestis KIM5 (YopM(+)) caused depletion of NK cells in the spleen, but not in the liver, and antibody-mediated ablation of NK cells had no effect on bacterial growth. There was no YopM-associated effect on the percentage of dendritic cells (DCs) or polymorphonuclear leukocytes (PMNs) in the early stage of infection; however, there was a YopM-associated effect on PMN integrity and on the influx of monocytes into the spleen. Ablation of Gr1(+) cells caused loss of the growth defect of YopM(-) Y. pestis in both the liver and spleen. In contrast, ablation of macrophages/DCs inhibited growth of both parent and mutant bacteria, accompanied by significantly fewer lesion sites in the liver. These results point toward PMNs and inflammatory monocytes as major cell types that control growth of YopM(-) Y. pestis. Infection with fully virulent Y. pestis CO92 and a YopM(-) derivative by intradermal and intranasal routes showed that the absence of YopM significantly increased the 50% lethal dose only in the intradermal model, suggesting a role for YopM in bubonic plague, in which acute inflammation occurs soon after infection.
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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.