ArticlePloS one2014
Neisseria gonorrhoeae modulates iron-limiting innate immune defenses in macrophages.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 59 citations in OpenAlex.
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- Mechanisms of host manipulation byFrontiers in microbiology · 2023Review
- Molecular Regulatory Mechanisms Drive Emergent Pathogenetic Properties ofMicroorganisms · 2022Review
- Stealthy microbes: HowFrontiers in cellular and infection microbiology · 2022Review
- Acclimation to Nutritional Immunity and Metal Intoxication Requires Zinc, Manganese, and Copper Homeostasis in the PathogenicFrontiers in cellular and infection microbiology · 2022Review
- Understanding the Potential and Risk of Bacterial Siderophores in Cancer.Frontiers in oncology · 2022Review
- Phenotypic Changes Associated WithFrontiers in cellular and infection microbiology · 2022Article
- Transcriptional and Translational Responsiveness of the Neisseria gonorrhoeae Type IV Secretion System to Conditions of Host Infections.Infection and immunity · 2021Article
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- Increasing Natural Resistance Associated Macrophage Protein 1 serum level after Miana treatment in BALB/c inducedAnnals of medicine and surgery (2012) · 2021Article
- Anti-Virulence Therapeutic Approaches forAntibiotics (Basel, Switzerland) · 2021Review
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- UPR modulation of host immunity by Pseudomonas aeruginosa in cystic fibrosis.Clinical science (London, England : 1979) · 2020Article
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- Identification of aPathogens (Basel, Switzerland) · 2020Article
- Inactivation of 3-hydroxybutyrate dehydrogenase type 2 promotes proliferation and metastasis of nasopharyngeal carcinoma by iron retention.British journal of cancer · 2020Article
- Immunomodulatory potential of polysaccharides fromVeterinary world · 2019Article
- LncRNA TP73-AS1 sponges miR-141-3p to promote the migration and invasion of pancreatic cancer cells through the up-regulation of BDH2.Bioscience reports · 2019Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Neisseria gonorrhoeae is a strict human pathogen that causes the sexually transmitted infection termed gonorrhea. The gonococcus can survive extracellularly and intracellularly, but in both environments the bacteria must acquire iron from host proteins for survival. However, upon infection the host uses a defensive response by limiting the bioavailability of iron by a number of mechanisms including the enhanced expression of hepcidin, the master iron-regulating hormone, which reduces iron uptake from the gut and retains iron in macrophages. The host also secretes the antibacterial protein NGAL, which sequesters bacterial siderophores and therefore inhibits bacterial growth. To learn whether intracellular gonococci can subvert this defensive response, we examined expression of host genes that encode proteins involved in modulating levels of intracellular iron. We found that N. gonorrhoeae can survive in association (tightly adherent and intracellular) with monocytes and macrophages and upregulates a panel of its iron-responsive genes in this environment. We also found that gonococcal infection of human monocytes or murine macrophages resulted in the upregulation of hepcidin, NGAL, and NRAMP1 as well as downregulation of the expression of the gene encoding the short chain 3-hydroxybutyrate dehydrogenase (BDH2); BDH2 catalyzes the production of the mammalian siderophore 2,5-DHBA involved in chelating and detoxifying iron. Based on these findings, we propose that N. gonorrhoeae can subvert the iron-limiting innate immune defenses to facilitate iron acquisition and intracellular survival.
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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.