ArticlePLoS pathogens2020
Mycobacterium abscessus infection leads to enhanced production of type 1 interferon and NLRP3 inflammasome activation in murine macrophages via mitochondrial oxidative stress.
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 59 papers.
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Who cites it
59 citing papers in PubMed, 80 citations in OpenAlex.
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- Punicalagin Enhances Autophagy Through Sirtuin 1/FoxO3a Axis to Inhibit Intracellular Mycobacterium Abscessus Infection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Molecular Mechanisms of cGAS-STING Axis and Mitochondrial Dysfunction-Related Diseases in Humans: A Comprehensive Review.Current neuropharmacology · 2026Review
- Pirenzepine exhibits anti-prostate cancer activity and enhances checkpoint inhibitor-based immunotherapy by targeting STING.European journal of medical research · 2025Article
- Pathogenicity and virulence ofVirulence · 2025Review
- MAB_0676c-induced enhanced IL-10 production inhibits the autophagic flux via the MTOR/RUBCN pathway.Virulence · 2025Article
- The Crosstalk BetweenCells · 2025Review
- PRRs-Dependent and Independent Mechanisms of STING Signaling in Inflammatory and Autoimmune Diseases.Biomedicines · 2025Review
- Corynebacterium pseudotuberculosis phospholipase D targets mitochondrial sphingomyelin and induces NLRP3-GSDMD axis-mediated pyroptosis in macrophages to promote infection.Veterinary research · 2025Article
- The role of colony morphotype in shaping gene essentiality inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Phage-mediated TLR2 signaling attenuates intracellular Mycobacterium abscessus survival in macrophages.Scientific reports · 2025Article
- Export of eDNA is a mechanism used by Mycobacterium avium subsp. hominissuis for survival within host macrophages.Archives of microbiology · 2025Article
- Insights on the Pathogenesis ofJournal of clinical medicine · 2025Review
- Next-generation rifamycins for the treatment of mycobacterial infections.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- 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
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium abscessus (MAB) is a rapidly growing mycobacterium (RGM), and infections with this pathogen have been increasing worldwide. Recently, we reported that rough type (MAB-R) but not smooth type (MAB-S) strains enhanced type 1 interferon (IFN-I) secretion via bacterial phagosome escape, contributing to increased virulence. Here, we sought to investigate the role of mitochondrial oxidative stress in bacterial survival, IFN-I secretion and NLRP3 inflammasome activation in MAB-infected murine macrophages. We found that live but not heat-killed (HK) MAB-R strains increased mitochondrial ROS (mtROS) and increased release of oxidized mitochondrial DNA (mtDNA) into the cytosol of murine macrophages compared to the effects of live MAB-S strains, resulting in enhanced NLRP3 inflammasome-mediated IL-1β and cGAS-STING-dependent IFN-I production. Treatment of the infected macrophages with mtROS-modulating agents such as mito-TEMPO or cyclosporin A reduced cytosolic oxidized mtDNA, which inhibited the MAB-R strain-induced production of IL-1β and IFN-I. The reduced cytosolic oxidized mtDNA also inhibited intracellular growth of MAB-R strains via cytosolic escape following phagosomal rupture and via IFN-I-mediated cell-to-cell spreading. Moreover, our data showed that mtROS-dependent IFN-I production inhibited IL-1β production, further contributing to MAB-R intracellular survival in murine macrophages. In conclusion, our data indicated that MAB-R strains enhanced IFN-I and IL-1β production by inducing mtROS as a pathogen-associated molecular pattern (PAMP). These events also enhance bacterial survival in macrophages and dampen inflammation, which contribute to the pathogenesis of MAB-R strains.
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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 Socratic graph.