ArticleJournal of leukocyte biology2014
Yersinia pestis survival and replication within human neutrophil phagosomes and uptake of infected neutrophils by macrophages.
Article in Journal of leukocyte biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 73 citations in OpenAlex.
- Plagued by the Past, Pressed by the Present: A One Health Perspective onBiomedicines · 2025Review
- Article
- "The NET effect": Neutrophil extracellular traps-a potential key component of the dysregulated host immune response in sepsis.Critical care (London, England) · 2025Review
- Brucella abortus impairs T lymphocyte responsiveness by mobilizing IL-1RA-secreting omental neutrophils.Nature communications · 2025Article
- Article
- Dying for a cause: The pathogenic manipulation of cell death and efferocytic pathways.Molecular oral microbiology · 2024Review
- Differential pathogenicity and lethality of bubonic plague (1720-1945) by sex, age and place.Proceedings. Biological sciences · 2024Article
- The Natural and Clinical History of Plague: From the Ancient Pandemics to Modern Insights.Microorganisms · 2024Review
- Pyroptosis in neutrophils: Multimodal integration of inflammasome and regulated cell death signaling pathways.Immunological reviews · 2023Review
- Article
- Unraveling the molecular determinants of the anti-phagocytic protein cloak of plague bacteria.PLoS pathogens · 2022Article
- Yersinia pestis antibiotic resistance: a systematic review.Osong public health and research perspectives · 2022Article
- Yersinia remodels epigenetic histone modifications in human macrophages.PLoS pathogens · 2021Article
- Finafloxacin Is an Effective Treatment for Inhalational Tularemia and Plague in Mouse Models of Infection.Antimicrobial agents and chemotherapy · 2021Article
- Antimicrobial Activity of Neutrophils Against Mycobacteria.Frontiers in immunology · 2021Review
- Encephalitozoon cuniculi takes advantage of efferocytosis to evade the immune response.PloS one · 2021Article
- The Diverse Roles of the Global Transcriptional Regulator PhoP in the Lifecycle ofPathogens (Basel, Switzerland) · 2020Review
- A Dual Role for the Plasminogen Activator Protease During the Preinflammatory Phase of Primary Pneumonic Plague.The Journal of infectious diseases · 2020Article
- Apoptosis inhibition by intracellular bacteria and its consequence on host immunity.Current opinion in immunology · 2019Review
- β-glucan-dependent shuttling of conidia from neutrophils to macrophages occurs during fungal infection establishment.PLoS biology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Yersinia pestis, the bacterial agent of plague, is transmitted by fleas. The bite of an infected flea deposits Y. pestis into the dermis and triggers recruitment of innate immune cells, including phagocytic PMNs. Y. pestis can subvert this PMN response and survive at the flea-bite site, disseminate, and persist in the host. Although its genome encodes a number of antiphagocytic virulence factors, phagocytosis of Y. pestis by PMNs has been observed. This study tests the hypotheses that Y. pestis, grown at the ambient temperature of the flea vector (21°C), where the major antiphagocytic virulence factors are not produced, can survive and replicate within human PMNs and can use PMNs as a route to infect macrophages subsequently. We show that Y. pestis is localized within PMN phagosomes, predominately as individual bacteria, and that intracellular bacteria can survive and replicate. Within 12 h of infection, ~70% of infected PMNs had PS on their surface and were plausibly competent for efferocytosis. With the use of live cell confocal imaging, we show that autologous HMDMs recognize and internalize infected PMNs and that Y. pestis survives and replicates within these HMDMs following efferocytosis. Addition of HMDMs to infected PMNs resulted in decreased secretion of inflammatory cytokines (compared with HMDMs incubated directly with pCD1(-) Y. pestis) and increased secretion of the anti-inflammatory cytokine IL-1ra. Thus, Y. pestis can survive and replicate within PMNs, and infected PMNs may be a route for noninflammatory infection of macrophages.
Indexed as
Identifiers
What OpenQuestion holds
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.