ArticlePLoS pathogens2020
Brucella suppress STING expression via miR-24 to enhance infection.
Article in PLoS pathogens, 2020. 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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Who cites it
24 citing papers in PubMed, 29 citations in OpenAlex.
- TLR9 DNA methylation and gene expression in cattle naturally infected with B. abortus.Tropical animal health and production · 2026Article
- MiR-1 mediates autophagy via ATG14 in sheep Leydig cells infected withFrontiers in veterinary science · 2026Article
- Extracellular vesicle microRNA signature as a highly accurate diagnostic biomarker for human brucellosis.Frontiers in cellular and infection microbiology · 2026Article
- Pathogenicity and virulence ofVirulence · 2025Review
- KSHV miRNAs target STING to evade innate immunity and facilitate KSHV lytic reactivation from latency.Cell reports · 2025Article
- Huc-MSCs-derived exosomes alleviate non-alcoholic steatohepatitis by regulating macrophages polarization through miR-24-3p/STING axis.Stem cell research & therapy · 2025Article
- In evolution's unending race: ancestral STING sensors inFrontiers in immunology · 2025Article
- Beyond survival to domination:Frontiers in microbiology · 2025Review
- The 4EHP-mediated translational repression of cGAS impedes the host immune response against DNA viruses.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- MiRNAs and lncRNAs in the regulation of innate immune signaling.Non-coding RNA research · 2023Review
- Japanese Flounder pol-miR-155 Is Involved inGenes · 2023Article
- Role of the cGAS/STING pathway in the control ofFrontiers in immunology · 2023Article
- Erratum to "Evolution of animal and human brucellosis in Algeria: a mini narrative review: Anerni n tawla n Malṭa n yiɣersiwen d yimdanen di Lezzayer: tasɣunt tanalasant tilemẓit" [New Microbes and New Infections March 46C, (2022) 100975].New microbes and new infections · 2022Article
- Immunosuppressive Mechanisms in Brucellosis in Light of Chronic Bacterial Diseases.Microorganisms · 2022Review
- Evolution of animal and human brucellosis in Algeria: a mini narrative review.New microbes and new infections · 2022Review
- Downregulation of Three Novel miRNAs in the Lymph Nodes of Sheep Immunized With theFrontiers in veterinary science · 2022Article
- Activation of mucosal immunity as a novel therapeutic strategy for combating brucellosis.Frontiers in microbiology · 2022Review
- Cell-Free DNA Promotes Inflammation in Patients With Oral Lichen PlanusFrontiers in immunology · 2022Article
- Review
- Galectin-3 regulates proinflammatory cytokine function and favours Brucella abortus chronic replication in macrophages and mice.Cellular microbiology · 2021Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
Brucellosis, caused by a number of Brucella species, remains the most prevalent zoonotic disease worldwide. Brucella establish chronic infections within host macrophages despite triggering cytosolic innate immune sensors, including Stimulator of Interferon Genes (STING), which potentially limit infection. In this study, STING was required for control of chronic Brucella infection in vivo. However, early during infection, Brucella down-regulated STING mRNA and protein. Down-regulation occurred post-transcriptionally, required live bacteria, the Brucella type IV secretion system, and was independent of host IRE1-RNase activity. STING suppression occurred in MyD88-/- macrophages and was not induced by Toll-like receptor agonists or purified Brucella lipopolysaccharide (LPS). Rather, Brucella induced a STING-targeting microRNA, miR-24-2, in a type IV secretion system-dependent manner. Furthermore, STING downregulation was inhibited by miR-24 anti-miRs and in Mirn23a locus-deficient macrophages. Failure to suppress STING expression in Mirn23a-/- macrophages correlated with diminished Brucella replication, and was rescued by exogenous miR-24. Mirn23a-/- mice were also more resistant to splenic colonization one week post infection. Anti-miR-24 potently suppressed replication in wild type, but much less in STING-/- macrophages, suggesting most of the impact of miR-24 induction on replication occurred via STING suppression. In summary, Brucella sabotages cytosolic surveillance by miR-24-dependent suppression of STING expression; post-STING activation "damage control" via targeted STING destruction may enable establishment of chronic infection.
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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.