ArticlePLoS pathogens2016
The Mechanism for Type I Interferon Induction by Mycobacterium tuberculosis is Bacterial Strain-Dependent.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 1 of them a synthesis that pooled it.
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Who cites it
117 citing papers in PubMed, 1 synthesis or guideline pooled it, 178 citations in OpenAlex.
- Global variation in bacterial strains that cause tuberculosis disease: a systematic review and meta-analysis.BMC medicine · 2018Pooled it
- Sequential inflammatory processes define human progression from M. tuberculosis infection to tuberculosis disease.PLoS pathogens · 2017Trial
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- Targeting cGAS-STING signaling to overcome antibiotic-resistant bacterial infections: Challenges and opportunities.Science advances · 2026Review
- Host mitochondrial DNA in bacterial pathogenesis: Friend, Foe, or Both?Archives of microbiology · 2026Review
- Macrophage adaptation to hypoxia in the tuberculous granuloma potentiates mycobacterium-induced mitochondrial damage and granuloma necrosis.bioRxiv : the preprint server for biology · 2026Article
- Molecular Mechanisms of cGAS-STING Axis and Mitochondrial Dysfunction-Related Diseases in Humans: A Comprehensive Review.Current neuropharmacology · 2026Review
- Mitochondria affect antibacterial immunity in cross talk with innate immune response molecules coded by genes of nuclear origin.Frontiers in immunology · 2026Article
- Pattern recognition receptors: function, regulation and therapeutic potential.Signal transduction and targeted therapy · 2025Review
- SIRT2 inhibition enhances mitochondrial apoptosis in Brucella-infected bovine placental trophoblast cells.Veterinary research · 2025Article
- Mitochondrial DNA signals driving immune responses: Why, How, Where?Cell communication and signaling : CCS · 2025Review
- For Better or Worse: Type I Interferon Responses in Bacterial Infection.Pathogens (Basel, Switzerland) · 2025Review
- In vivo regulation of the monocyte phenotype by Mycobacterium marinum and the ESX-1 type VII secretion system.Scientific reports · 2025Article
- The STING signaling pathways and bacterial infection.Apoptosis : an international journal on programmed cell death · 2025Review
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
- Comparative transcriptomic analysis of mouse macrophages infected with live attenuated vaccine strains ofFrontiers in immunology · 2025Article
- Mitochondrial dysfunction in acute and post-acute phases of COVID-19 and risk of non-communicable diseases.npj metabolic health and disease · 2024Review
- Cytosolic serpins act in a cytoprotective feedback loop that limits ESX-1-dependent death ofmBio · 2024Article
57 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Type I interferons (including IFNαβ) are innate cytokines that may contribute to pathogenesis during Mycobacterium tuberculosis (Mtb) infection. To induce IFNβ, Mtb must gain access to the host cytosol and trigger stimulator of interferon genes (STING) signaling. A recently proposed model suggests that Mtb triggers STING signaling through bacterial DNA binding cyclic GMP-AMP synthase (cGAS) in the cytosol. The aim of this study was to test the generalizability of this model using phylogenetically distinct strains of the Mtb complex (MTBC). We infected bone marrow derived macrophages with strains from MTBC Lineages 2, 4 and 6. We found that the Lineage 6 strain induced less IFNβ, and that the Lineage 2 strain induced more IFNβ, than the Lineage 4 strain. The strains did not differ in their access to the host cytosol and IFNβ induction by each strain required both STING and cGAS. We also found that the three strains shed similar amounts of bacterial DNA. Interestingly, we found that the Lineage 6 strain was associated with less mitochondrial stress and less mitochondrial DNA (mtDNA) in the cytosol compared with the Lineage 4 strain. Treating macrophages with a mitochondria-specific antioxidant reduced cytosolic mtDNA and inhibited IFNβ induction by the Lineage 2 and 4 strains. We also found that the Lineage 2 strain did not induce more mitochondrial stress than the Lineage 4 strain, suggesting that additional pathways contribute to higher IFNβ induction. These results indicate that the mechanism for IFNβ by Mtb is more complex than the established model suggests. We show that mitochondrial dynamics and mtDNA contribute to IFNβ induction by Mtb. Moreover, we show that the contribution of mtDNA to the IFNβ response varies by MTBC strain and that additional mechanisms exist for Mtb to induce IFNβ.
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