ArticleBMC immunology2010
YopH inhibits early pro-inflammatory cytokine responses during plague pneumonia.
Article in BMC immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 31 citations in OpenAlex.
- Selective Inhibition ofPharmaceutics · 2025Article
- Pathogenicity and virulence ofVirulence · 2024Review
- Type 3 secretion system induced leukotriene B4 synthesis by leukocytes is actively inhibited by Yersinia pestis to evade early immune recognition.PLoS pathogens · 2024Article
- 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
- Modeling Pneumonic Plague in Human Precision-Cut Lung Slices Highlights a Role for the Plasminogen Activator Protease in Facilitating Type 3 Secretion.Infection and immunity · 2019Article
- Article
- 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
- Immunomodulatory Yersinia outer proteins (Yops)-useful tools for bacteria and humans alike.Virulence · 2017Review
- 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
- Role of the Yersinia YopJ protein in suppressing interleukin-8 secretion by human polymorphonuclear leukocytes.Microbes and infection · 2016Article
- Circumventing Y. pestis Virulence by Early Recruitment of Neutrophils to the Lungs during Pneumonic Plague.PLoS pathogens · 2015Article
- Yersinia pestis activates both IL-1β and IL-1 receptor antagonist to modulate lung inflammation during pneumonic plague.PLoS pathogens · 2015Article
- Yersinia pestis survival and replication within human neutrophil phagosomes and uptake of infected neutrophils by macrophages.Journal of leukocyte biology · 2014Article
- Early apoptosis of macrophages modulated by injection of Yersinia pestis YopK promotes progression of primary pneumonic plague.PLoS pathogens · 2013Article
- Pulmonary infection by Yersinia pestis rapidly establishes a permissive environment for microbial proliferation.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Article
- Article
- Host Defense and the Airway Epithelium: Frontline Responses That Protect against Bacterial Invasion and Pneumonia.Journal of pathogens · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundYersinia pestis is the causative agent of pneumonic plague; recently, we and others reported that during the first 24-36 hours after pulmonary infection with Y. pestis pro-inflammatory cytokine expression is undetectable in lung tissues.
resultsHere, we report that, intranasal infection of mice with CO92 delta yopH mutant results in an early pro-inflammatory response in the lungs characterized by an increase in the pro-inflammatory cytokines Tumor Necrosis Factor-alpha and Interleukin one-beta 24 hours post-infection. CO92 delta yopH colonizes the lung but does not disseminate to the liver or spleen and is cleared from the host within 72 hours post-infection. This is different from what is observed in a wild-type CO92 infection, where pro-inflammatory cytokine expression and immune cell infiltration into the lungs is not detectable until 36-48 h post-infection. CO92 rapidly disseminates to the liver and spleen resulting in high bacterial burdens in these tissues ultimately cumulating in death 72-94 h post-infection. Mice deficient in TNF-alpha are more susceptible to CO92 delta yopH infection with 40% of the mice succumbing to infection.
conclusionsAltogether, our results suggest that YopH can inhibit an early pro-inflammatory response in the lungs of mice and that this is an important step in the pathogenesis of 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.