ArticleMediators of inflammation2013
Neisseria gonorrhoeae induces a tolerogenic phenotype in macrophages to modulate host immunity.
Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Characterization ofFrontiers in cellular and infection microbiology · 2024Article
- Article
- Commensal Neisseria species share immune suppressive mechanisms with Neisseria gonorrhoeae.PloS one · 2023Article
- Mechanisms of host manipulation byFrontiers in microbiology · 2023Review
- Fascinating Molecular and Immune Escape Mechanisms in the Treatment of STIs (Syphilis, Gonorrhea, Chlamydia, and Herpes Simplex).International journal of molecular sciences · 2022Review
- Tissue Models forFrontiers in cellular and infection microbiology · 2022Review
- Systemic and Mucosal Concentrations of Nine Cytokines Among Individuals withAAS open research · 2022Article
- Vaccine Candidates for the Control and Prevention of the Sexually Transmitted Disease Gonorrhea.Vaccines · 2021Review
- A novel gonorrhea vaccine composed of MetQ lipoprotein formulated with CpG shortens experimental murine infection.Vaccine · 2020Article
- Pathogenesis ofFrontiers in immunology · 2018Review
- Macrophage-Frontiers in immunology · 2018Review
- Proteomics, Bioinformatics and Structure-Function Antigen Mining For Gonorrhea Vaccines.Frontiers in immunology · 2018Review
- Neisseria gonorrhoeae survives within and modulates apoptosis and inflammatory cytokine production of human macrophages.Cellular microbiology · 2016Article
- Association Between Reduced Risk of Intracerebral Hemorrhage and Pelvic Inflammatory Disease.Medicine · 2016Observational
- ATP Induces IL-1Mediators of inflammation · 2016Article
- Neisseria gonorrhoeae Modulates Immunity by Polarizing Human Macrophages to a M2 Profile.PloS one · 2015Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neisseria gonorrhoeae is the etiological agent of gonorrhoea, which is a sexually transmitted disease widespread throughout the world. N. gonorrhoeae does not improve immune response in patients with reinfection, suggesting that gonococcus displays several mechanisms to evade immune response and survive in the host. N. gonorrhoeae is able to suppress the protective immune response at different levels, such as B and T lymphocytes and dendritic cells. In this study, we determined whether N. gonorrhoeae directly conditions the phenotype of RAW 264.7 murine macrophage cell line and its response. We established that gonococcus was effectively phagocytosed by the RAW 264.7 cells and upregulates production of immunoregulatory cytokines (IL-10 and TGF- β 1) but not the production of proinflammatory cytokine TNF- α , indicating that gonococcus induces a shift towards anti-inflammatory cytokine production. Moreover, N. gonorrhoeae did not induce significant upregulation of costimulatory CD86 and MHC class II molecules. We also showed that N. gonorrhoeae infected macrophage cell line fails to elicit proliferative CD4+ response. This implies that macrophage that can phagocytose gonococcus do not display proper antigen-presenting functions. These results indicate that N. gonorrhoeae induces a tolerogenic phenotype in antigen-presenting cells, which seems to be one of the mechanisms to induce evasion of immune response.
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