ArticlePLoS pathogens2013
Neutrophils exert a suppressive effect on Th1 responses to intracellular pathogen Brucella abortus.
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 24 papers.
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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
24 citing papers in PubMed, 42 citations in OpenAlex.
- Brucella abortus interferes with the inflammatory response and tissue repair in mice.Scientific reports · 2025Article
- Reactivation of hidden-latentAntimicrobial agents and chemotherapy · 2025Article
- β-Glucan reprograms neutrophils to promote disease tolerance against influenza A virus.Nature immunology · 2025Article
- Brucella abortus impairs T lymphocyte responsiveness by mobilizing IL-1RA-secreting omental neutrophils.Nature communications · 2025Article
- STK11 mutation affects tumor proliferation by impacting CD4Central-European journal of immunology · 2024Article
- Immunosuppressive Mechanisms in Brucellosis in Light of Chronic Bacterial Diseases.Microorganisms · 2022Review
- The Role of Neutrophils in Brucellosis.Microbiology and molecular biology reviews : MMBR · 2020Review
- The regulatory roles of neutrophils in adaptive immunity.Cell communication and signaling : CCS · 2019Review
- Article
- Neutrophils Dampen Adaptive Immunity in Brucellosis.Infection and immunity · 2019Article
- Neutrophils as Trojan Horse Vehicles forFrontiers in immunology · 2019Article
- Depletion of Complement Enhances the Clearance of Brucella abortus in Mice.Infection and immunity · 2018Article
- Immunogenicity evaluation of plasmids encodingIranian journal of basic medical sciences · 2018Article
- Persistence ofJournal of immunology research · 2018Article
- Allergic Asthma FavorsFrontiers in immunology · 2018Article
- Contribution of IL-1RI Signaling to Protection againstFrontiers in immunology · 2017Article
- CXCR2 Mediates Brucella-Induced Arthritis in Interferon γ-Deficient Mice.The Journal of infectious diseases · 2016Article
- N-Formyl-Perosamine Surface Homopolysaccharides Hinder the Recognition of Brucella abortus by Mouse Neutrophils.Infection and immunity · 2016Article
- Rapid Sequestration of Leishmania mexicana by Neutrophils Contributes to the Development of Chronic Lesion.PLoS pathogens · 2015Article
- Brucella abortus Induces the Premature Death of Human Neutrophils through the Action of Its Lipopolysaccharide.PLoS pathogens · 2015Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polymorphonuclear neutrophils (PMNs) are the first line of defense against microbial pathogens. In addition to their role in innate immunity, PMNs may also regulate events related to adaptive immunity. To investigate the influence of PMNs in the immune response during chronic bacterial infections, we explored the course of brucellosis in antibody PMN-depleted C57BL/6 mice and in neutropenic mutant Genista mouse model. We demonstrate that at later times of infection, Brucella abortus is killed more efficiently in the absence of PMNs than in their presence. The higher bacterial removal was concomitant to the: i) comparatively reduced spleen swelling; ii) augmented infiltration of epithelioid histiocytes corresponding to macrophages/dendritic cells (DCs); iii) higher recruitment of monocytes and monocyte/DCs phenotype; iv) significant activation of B and T lymphocytes, and v) increased levels of INF-γ and negligible levels of IL4 indicating a balance of Th1 over Th2 response. These results reveal that PMNs have an unexpected influence in dampening the immune response against intracellular Brucella infection and strengthen the notion that PMNs actively participate in regulatory circuits shaping both innate and adaptive immunity.
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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.