ArticleVirulence2017
cGAS-STING-TBK1-IRF3/7 induced interferon-β contributes to the clearing of non tuberculous mycobacterial infection in mice.
Article in Virulence, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 45 citations in OpenAlex.
- Purine and pyrimidine-based bacterial cyclic dinucleotides egress the phagosome and activate the innate immune sensor STING.Immunity · 2026Article
- ATP6AP2 ameliorates inflammation and pyroptosis in heart failure by promoting lysosome-dependent STING degradation.Apoptosis : an international journal on programmed cell death · 2026Article
- Organelle interplay in host responses and mycobacterial resilience.EMBO reports · 2026Review
- Nano-in-Micro GelMA depots assist electro-thermal-immuno orchestral treatment for solid triple negative breast tumor.Materials today. Bio · 2026Article
- Proton-activated chloride channel governs phagosome-mediated antibacterial immunity in peritoneal macrophages.The Journal of experimental medicine · 2025Article
- Mycobacterium tuberculosis Infection of Retinal Endothelial Cells Induces Interferon Signaling Activation: Insights Into Tubercular Retinal Vasculitis.Investigative ophthalmology & visual science · 2025Article
- Phagosome-mediated anti-bacterial immunity is governed by the proton-activated chloride channel in peritoneal macrophages.bioRxiv : the preprint server for biology · 2025Article
- The antiviral activity of myricetin against pseudorabies virus through regulation of the type I interferon signaling pathway.Journal of virology · 2025Article
- The regulation of cGAS-STING signaling by RNA virus-derived components.Virology journal · 2024Review
- Article
- cGAS Mediates the Inflammatory Responses of Human Microglial Cells to Genotoxic DNA Damage.Inflammation · 2024Article
- STING dependent BAX-IRF3 signaling results in apoptosis during late-stage Coxiella burnetii infection.Cell death & disease · 2024Article
- Activation of host nucleic acid sensors byCritical reviews in microbiology · 2024Review
- Article
- Activated cGAS/STING signaling elicits endothelial cell senescence in early diabetic retinopathy.JCI insight · 2023Article
- Endogenous Retroviruses as Modulators of Innate Immunity.Pathogens (Basel, Switzerland) · 2023Review
- Interferon regulatory factor 7 in inflammation, cancer and infection.Frontiers in immunology · 2023Review
- LncRNA PCAT1 activates SOX2 and suppresses radioimmune responses via regulating cGAS/STING signalling in non-small cell lung cancer.Clinical and translational medicine · 2022Article
- DNA damage repair promotion in colonic epithelial cells by andrographolide downregulated cGAS‒STING pathway activation and contributed to the relief of CPT-11-induced intestinal mucositis.Acta pharmaceutica Sinica. B · 2022Article
- cGAS-STING-mediated IFN-I Response in Host Defense and Neuroinflammatory Diseases.Current neuropharmacology · 2022Review
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type I interferons (IFN-I), such as IFN-α and IFN-β are important messengers in the host response against bacterial infections. Knowledge about the role of IFN-I in infections by nontuberculous mycobacteria (NTM) is limited. Here we show that macrophages infected with pathogens of the Mycobacterium avium complex produced significantly lower amounts of IFN-β than macrophages infected with the opportunistic pathogen M. smegmatis. To dissect the molecular mechanisms of this phenomenon, we focused on the obligate pathogen Mycobacterium avium ssp paratuberculosis (MAP) and the opportunistic M. smegmatis. Viability of both bacteria was required for induction of IFN-β in macrophages. Both bacteria induced IFN-β via the cGAS-STING-TBK1-IRF3/7-pathway of IFN-β activation. Stronger phosphorylation of TBK1 and higher amounts of extracellular bacterial DNA in the macrophage cytosol were found in M. smegmatis infected macrophages than in MAP infected macrophages. After intraperitoneal infection of mice, a strong Ifnb induction by M. smegmatis correlated with clearance of the bacteria. In contrast, MAP only induced weak Ifnb expression which correlated with bacterial persistence and increased number of granulomas in the liver. In mice lacking the type I interferon receptor we observed improved survival of M. smegmatis while survival of MAP was similar to that in wildtype mice. On the other hand, treatment of MAP infected wildtype mice with the IFN-I inducer poly(I:C) or recombinant IFN-β impaired the survival of MAP. This indicates an essential role of IFN-I in clearing infections by MAP and M. smegmatis. The expression level of IFN-I is decisive for transient versus persistent NTM infection.
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