ArticlePloS one2011
MyD88 and STING signaling pathways are required for IRF3-mediated IFN-β induction in response to Brucella abortus infection.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed, 81 citations in OpenAlex.
- Polymorphisms in IRF3 exon 1 influence the immune response to Brucella infection in small ruminants.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Signal Transducers and Activators of Transcription 1 (STAT1), STAT2, and T Cells Mediate Interferon-Dependent Protection Against Neurobrucellosis.The Journal of infectious diseases · 2026Article
- Pathogenicity and virulence ofVirulence · 2025Review
- Brucella abortus induces dynamin-related protein 1 (DRP1)-dependent mitochondrial fission in infected macrophages via stress sensor IRE1α altering metabolic function.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- The dual role of type I interferons in bacterial infections: from immune defense to pathogenesis.mBio · 2025Review
- MyD88 signalling in B cells and antibody responses during Oropouche virus-induced neurological disease in mice.EBioMedicine · 2025Article
- For Better or Worse: Type I Interferon Responses in Bacterial Infection.Pathogens (Basel, Switzerland) · 2025Review
- Type I interferons regulate nitric oxide production inFrontiers in immunology · 2025Article
- Virion-incorporated CD14 enables HIV-1 to bind LPS and initiate TLR4 signaling in immune cells.Journal of virology · 2024Article
- ZBP1 sensesFrontiers in immunology · 2024Article
- Innate Lymphoid Cells and Interferons Limit Neurologic and Articular Complications of Brucellosis.The American journal of pathology · 2023Article
- A TLR4 agonist liposome formulation effectively stimulates innate immunity and enhances protection from bacterial infection.Innate immunity · 2023Article
- Role of the cGAS/STING pathway in the control ofFrontiers in immunology · 2023Article
- Immunosuppressive Mechanisms in Brucellosis in Light of Chronic Bacterial Diseases.Microorganisms · 2022Review
- Activation of mucosal immunity as a novel therapeutic strategy for combating brucellosis.Frontiers in microbiology · 2022Review
- Review
- Galectin-3 regulates proinflammatory cytokine function and favours Brucella abortus chronic replication in macrophages and mice.Cellular microbiology · 2021Article
- Impact of Type I Interferons on Susceptibility to Bacterial Pathogens.Trends in microbiology · 2021Review
- Epitope-Based Vaccine of aFrontiers in immunology · 2021Article
- ASC-Mediated Inflammation and Pyroptosis AttenuatesPathogens (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type I interferons (IFNs) are cytokines that orchestrate diverse immune responses to viral and bacterial infections. Although typically considered to be most important molecules in response to viruses, type I IFNs are also induced by most, if not all, bacterial pathogens. In this study, we addressed the role of type I IFN signaling during Brucella abortus infection, a facultative intracellular bacterial pathogen that causes abortion in domestic animals and undulant fever in humans. Herein, we have shown that B. abortus induced IFN-β in macrophages and splenocytes. Further, IFN-β induction by Brucella was mediated by IRF3 signaling pathway and activates IFN-stimulated genes via STAT1 phosphorylation. In addition, IFN-β expression induced by Brucella is independent of TLRs and TRIF signaling but MyD88-dependent, a pathway not yet described for Gram-negative bacteria. Furthermore, we have identified Brucella DNA as the major bacterial component to induce IFN-β and our study revealed that this molecule operates through a mechanism dependent on RNA polymerase III to be sensed probably by an unknown receptor via the adaptor molecule STING. Finally, we have demonstrated that IFN-αβR KO mice are more resistant to infection suggesting that type I IFN signaling is detrimental to host control of Brucella. This resistance phenotype is accompanied by increased IFN-γ and NO production by IFN-αβR KO spleen cells and reduced apoptosis.
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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.