ArticleInfection and immunity2007
Brucella suis prevents human dendritic cell maturation and antigen presentation through regulation of tumor necrosis factor alpha secretion.
Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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Who cites it
42 citing papers in PubMed, 84 citations in OpenAlex.
- Complementary Use of Probiotics and Their Antimicrobial Proteins in Brucellosis: A Comprehensive Review of Mechanisms and Clinical Benefits.Probiotics and antimicrobial proteins · 2026Review
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- Review
- Spatiotemporal dynamics of Brucella immune evasion across infection stages.Frontiers in immunology · 2025Review
- Exploring potential cytokine profiles as diagnostic biomarkers for brucellosis in Mediterranean Buffaloes.Frontiers in veterinary science · 2025Article
- Review
- Origins of symbiosis: shared mechanisms underlying microbial pathogenesis, commensalism and mutualism of plants and animals.FEMS microbiology reviews · 2023Review
- Pal Affects the Proliferation in Macrophages and Virulence of Brucella, and as Mucosal Adjuvants, Provides an Effective Protection to Mice Against Salmonella Enteritidis.Current microbiology · 2022Article
- Immunosuppressive Mechanisms in Brucellosis in Light of Chronic Bacterial Diseases.Microorganisms · 2022Review
- Tumor Necrosis Factor Alpha Contributes to Inflammatory Pathology in the Placenta during Brucella abortus Infection.Infection and immunity · 2022Article
- A gene expression map of host immune response in human brucellosis.Frontiers in immunology · 2022Article
- microRNAs in human brucellosis: A promising therapeutic approach and biomarker for diagnosis and treatment.Immunity, inflammation and disease · 2021Review
- Uncovering the Hidden Credentials ofMicrobiology and molecular biology reviews : MMBR · 2021Review
- Dendritic cells and Brucella spp. interaction: the sentinel host and the stealthy pathogen.Folia microbiologica · 2020Review
- Astragalus polysaccharide strengthens the inflammatory and immune responses ofExperimental and therapeutic medicine · 2019Article
- Article
- Variability in the response of canine and human dendritic cells stimulated with Brucella canis.Veterinary research · 2017Article
- Identification ofFrontiers in microbiology · 2017Article
- Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brucella is a facultative intracellular pathogen and the etiological agent of brucellosis. In some cases, human brucellosis results in a persistent infection that may reactivate years after the initial exposure. The mechanisms by which the parasite evades clearance by the immune response to chronically infect its host are unknown. We recently demonstrated that dendritic cells (DCs), which are critical components of adaptive immunity, are highly susceptible to Brucella infection and are a preferential niche for the development of the bacteria. Here, we report that in contrast to several intracellular bacteria, Brucella prevented the infected DCs from engaging in their maturation process and impaired their capacities to present antigen to naïve T cells and to secrete interleukin-12. Moreover, Brucella-infected DCs failed to release tumor necrosis factor alpha (TNF-alpha), a defect involving the bacterial protein Omp25. Exogenous TNF-alpha addition to Brucella-infected DCs restored cell maturation and allowed them to present antigens. Two avirulent mutants of B. suis, B. suis bvrR and B. suis omp25 mutants, which do not express the Omp25 protein, triggered TNF-alpha production upon DC invasion. Cells infected with these mutants subsequently matured and acquired the ability to present antigens, two properties which were dramatically impaired by addition of anti-TNF-alpha antibodies. In light of these data, we propose a model in which virulent Brucella alters the maturation and functions of DCs through Omp25-dependent control of TNF-alpha production. This model defines a specific evasion strategy of the bacteria by which they can escape the immune response to chronically infect their host.
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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.